PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 20368434-0 2010 Clinical response and miR-29b predictive significance in older AML patients treated with a 10-day schedule of decitabine. Decitabine 110-120 microRNA 29b-1 Homo sapiens 22-29 20564213-8 2010 Treatment with the hedgehog inhibitor cyclopamine, which blocks smoothened signaling, increased the activity of the promoter and expression of mature mir-29b. cyclopamine 38-49 microRNA 29b-1 Homo sapiens 150-157 21951844-7 2011 Adenovirus-mediated overexpression of miR-29b induced apoptosis and elevated caspase-3 activation in HMCLs. hmcls 101-106 microRNA 29b-1 Homo sapiens 38-45 20368434-14 2010 Levels of miR-29b should be validated as a predictive factor for stratification of older AML patients to decitabine treatment. Decitabine 105-115 microRNA 29b-1 Homo sapiens 10-17 19509563-4 2009 miR-29b expression was analyzed using quantitative stem-loop reverse transcriptase polymerase chain reaction on a set of 50 formalin-fixed, paraffin-embedded ovarian serous carcinoma samples. Formaldehyde 124-132 microRNA 29b-1 Homo sapiens 0-7 19966860-7 2010 miR-29b locked nucleic acid (LNA) antisense oligonucleotide transfection into LMP1-expressing cells reduced miR-29b expression and consequently reconstituted TCL1, suggesting that LMP1 negatively regulates TCL1 through miR-29b upregulation. Oligonucleotides 44-59 microRNA 29b-1 Homo sapiens 0-7 19966860-7 2010 miR-29b locked nucleic acid (LNA) antisense oligonucleotide transfection into LMP1-expressing cells reduced miR-29b expression and consequently reconstituted TCL1, suggesting that LMP1 negatively regulates TCL1 through miR-29b upregulation. Oligonucleotides 44-59 microRNA 29b-1 Homo sapiens 108-115 19966860-7 2010 miR-29b locked nucleic acid (LNA) antisense oligonucleotide transfection into LMP1-expressing cells reduced miR-29b expression and consequently reconstituted TCL1, suggesting that LMP1 negatively regulates TCL1 through miR-29b upregulation. Oligonucleotides 44-59 microRNA 29b-1 Homo sapiens 108-115 19850741-7 2009 Together, the data support a tumor suppressor role for miR-29 and provide a rationale for the use of synthetic miR-29b oligonucleotides as a novel strategy to improve treatment response in AML. Oligonucleotides 119-135 microRNA 29b-1 Homo sapiens 111-118 19956414-12 2009 MiR-29b increased cell viability under both chronic oxidative stress and physiologic oxygen concentrations. Oxygen 85-91 microRNA 29b-1 Homo sapiens 0-7 19509563-4 2009 miR-29b expression was analyzed using quantitative stem-loop reverse transcriptase polymerase chain reaction on a set of 50 formalin-fixed, paraffin-embedded ovarian serous carcinoma samples. Paraffin 140-148 microRNA 29b-1 Homo sapiens 0-7 34667723-0 2021 Exosomal miR-29b found in aqueous humour mediates calcium signaling in diabetic patients with cataract. Calcium 50-57 microRNA 29b-1 Homo sapiens 9-16 17204650-5 2007 The distinctive hexanucleotide terminal motif of miR-29b acts as a transferable nuclear localization element that directs nuclear enrichment of miRNAs or small interfering RNAs to which it is attached. hexanucleotide 16-30 microRNA 29b-1 Homo sapiens 49-56 30840264-7 2019 We also found that exogenous miR-29b reduces the proliferation, promotes the apoptosis and upregulates the sensitivity to chemotherapy (doxorubicin) of osteosarcoma cells via direct targeting of the MMP-9. Doxorubicin 136-147 microRNA 29b-1 Homo sapiens 29-36 34618275-7 2021 This study discovers the mechanism that Sus and SS promote BTCs EMT by YAP through miR-29b posttranscriptionally and highlight the potential of YAP and miR-29b in tumor therapy. 2-Deoxy-3,6-Di-O-Sulfo-2-(Sulfoamino)-Alpha-D-Glucopyranose 40-43 microRNA 29b-1 Homo sapiens 83-90 34618275-7 2021 This study discovers the mechanism that Sus and SS promote BTCs EMT by YAP through miR-29b posttranscriptionally and highlight the potential of YAP and miR-29b in tumor therapy. 2-Deoxy-3,6-Di-O-Sulfo-2-(Sulfoamino)-Alpha-D-Glucopyranose 40-43 microRNA 29b-1 Homo sapiens 152-159 34618275-7 2021 This study discovers the mechanism that Sus and SS promote BTCs EMT by YAP through miR-29b posttranscriptionally and highlight the potential of YAP and miR-29b in tumor therapy. H-SER-SER-OH 48-50 microRNA 29b-1 Homo sapiens 83-90 34618275-7 2021 This study discovers the mechanism that Sus and SS promote BTCs EMT by YAP through miR-29b posttranscriptionally and highlight the potential of YAP and miR-29b in tumor therapy. H-SER-SER-OH 48-50 microRNA 29b-1 Homo sapiens 152-159 34997082-10 2022 MiR-29b inhibits TGF-beta1 induced MMT and replacement of miR-29b in the peritoneal cavity might be effective to prevent development of PM partly through the effects on MC. pipermethystine 136-138 microRNA 29b-1 Homo sapiens 58-65 34377003-9 2021 Furthermore, miR-29b suppressed HREC proliferation and migration under high-glucose stimulation, which was significantly attenuated by enforced expression of SERPINH1. Glucose 76-83 microRNA 29b-1 Homo sapiens 13-20 34377003-11 2021 Further mechanistic studies indicated that miR-29b/SERPINH1 signaling participated in high glucose-induced enhancement in the proliferation and migration of HRECs. Glucose 91-98 microRNA 29b-1 Homo sapiens 43-50 35627221-2 2022 In particular, cigarette smoke and tea polyphenols may influence DNMT3B mRNA expression by regulating microRNA (miR)-29b expression. Polyphenols 39-50 microRNA 29b-1 Homo sapiens 102-120 34639119-8 2021 Treatment with HLSC-EVs caused increased expression of miR29b, which was significantly inhibited in the presence of alpha-amanitin. Alpha-Amanitin 116-130 microRNA 29b-1 Homo sapiens 55-61 34159768-6 2021 Moreover, rescue experiments found that IL-22 neutralized the repressive effects of miR-29b on Th17/Treg ratio and inflammatory response. treg 100-104 microRNA 29b-1 Homo sapiens 84-91 34997082-10 2022 MiR-29b inhibits TGF-beta1 induced MMT and replacement of miR-29b in the peritoneal cavity might be effective to prevent development of PM partly through the effects on MC. Methylcholanthrene 169-171 microRNA 29b-1 Homo sapiens 58-65 32275350-10 2021 Furthermore, up-regulation of miR-29b was able to potentiate the level of anti-tumor activity of TMZ against tested cells. Temozolomide 97-100 microRNA 29b-1 Homo sapiens 30-37 34967279-0 2022 Long noncoding RNA Gm44593 attenuates oxidative stress from age-related hearing loss by regulating miR-29b/WNK1. gm44593 19-26 microRNA 29b-1 Homo sapiens 99-106 34967279-8 2022 We also proved that miR-29b is the direct target of lncRNA Gm44593. gm44593 59-66 microRNA 29b-1 Homo sapiens 20-27 34967279-9 2022 Overexpression of miR-29b completely restored the effect induced by lncRNA Gm44593. gm44593 75-82 microRNA 29b-1 Homo sapiens 18-25 34057209-13 2021 In addition, long-term nicotine or CSC exposure reduced miR-29b and miR-199a expression to less than 50% of that in the unstimulated HGFs. Nicotine 23-31 microRNA 29b-1 Homo sapiens 56-63 33740985-0 2021 Effects of metal nanoparticles on tight junction-associated proteins via HIF-1alpha/miR-29b/MMPs pathway in human epidermal keratinocytes. Metals 11-16 microRNA 29b-1 Homo sapiens 84-91 33740985-4 2021 In this study, we proposed that exposure of human epidermal keratinocytes (HaCaT) to metal nanoparticles, such as nickel nanoparticles, dysregulates tight-junction associated proteins by interacting with the HIF-1alpha/miR-29b/MMPs axis. Metals 85-90 microRNA 29b-1 Homo sapiens 219-226 33740985-4 2021 In this study, we proposed that exposure of human epidermal keratinocytes (HaCaT) to metal nanoparticles, such as nickel nanoparticles, dysregulates tight-junction associated proteins by interacting with the HIF-1alpha/miR-29b/MMPs axis. Nickel 114-120 microRNA 29b-1 Homo sapiens 219-226 33740985-15 2021 Pretreatment of cells with a HIF-1alpha inhibitor, CAY10585, abolished Nano-Ni-induced miR-29b down-regulation and MMP-2/9 up-regulation. LW6 51-59 microRNA 29b-1 Homo sapiens 87-94 32275350-11 2021 We also found that autophagy induced by miR-29b, at least partially, contributed to the increase of TMZ sensitivity in GBM cells. Temozolomide 100-103 microRNA 29b-1 Homo sapiens 40-47 32275350-13 2021 Consistent with observations in vitro, findings ofin vivo assessment also confirmed that overexpression of miR-29b was able to effectively halt tumor growth and enhance the anti-tumor activity of TMZ. Temozolomide 196-199 microRNA 29b-1 Homo sapiens 107-114 32275350-14 2021 CONCLUSION: miR-29b potentiates TMZ sensitivity against GBM cells by inducing autophagy and the combined use of miR-29 mimic and TMZ might represent a potential therapeutic strategy for GBM patients. Temozolomide 32-35 microRNA 29b-1 Homo sapiens 12-19 32746845-0 2020 C6-ceramide treatment inhibits the proangiogenic activity of multiple myeloma exosomes via the miR-29b/Akt pathway. N-caproylsphingosine 0-11 microRNA 29b-1 Homo sapiens 95-102 32054316-3 2020 Exosomes isolated from cells treated with HNESC exhibited the strongest inhibitory effect on cell apoptosis while exhibiting the highest level of miR-29b expression and the lowest levels of PTEN and caspase-3 expression. hnesc 42-47 microRNA 29b-1 Homo sapiens 146-153 32054316-5 2020 The exosomes isolated from the groups of HNESC and HNESC + miR-29b mimics exhibited in vivo therapeutic effects by restoring the BBB score and apoptosis index of post-SCI neuron cells to those of normal neuron cells, with the exosomes collected from the group of HNESC + miR-29b mimics showing the strongest effect. hnesc 41-46 microRNA 29b-1 Homo sapiens 271-278 32054316-5 2020 The exosomes isolated from the groups of HNESC and HNESC + miR-29b mimics exhibited in vivo therapeutic effects by restoring the BBB score and apoptosis index of post-SCI neuron cells to those of normal neuron cells, with the exosomes collected from the group of HNESC + miR-29b mimics showing the strongest effect. hnesc 51-56 microRNA 29b-1 Homo sapiens 59-66 32054316-5 2020 The exosomes isolated from the groups of HNESC and HNESC + miR-29b mimics exhibited in vivo therapeutic effects by restoring the BBB score and apoptosis index of post-SCI neuron cells to those of normal neuron cells, with the exosomes collected from the group of HNESC + miR-29b mimics showing the strongest effect. hnesc 51-56 microRNA 29b-1 Homo sapiens 271-278 32054316-5 2020 The exosomes isolated from the groups of HNESC and HNESC + miR-29b mimics exhibited in vivo therapeutic effects by restoring the BBB score and apoptosis index of post-SCI neuron cells to those of normal neuron cells, with the exosomes collected from the group of HNESC + miR-29b mimics showing the strongest effect. hnesc 51-56 microRNA 29b-1 Homo sapiens 59-66 32054316-5 2020 The exosomes isolated from the groups of HNESC and HNESC + miR-29b mimics exhibited in vivo therapeutic effects by restoring the BBB score and apoptosis index of post-SCI neuron cells to those of normal neuron cells, with the exosomes collected from the group of HNESC + miR-29b mimics showing the strongest effect. hnesc 51-56 microRNA 29b-1 Homo sapiens 271-278 33261656-13 2020 Furthermore, circ6401 was found to bind to miR-29b-1-5p and prevent it from decreasing the level of RAP1B, a crucial protein involved in the VEGF signaling pathway, which promoted angiogenesis and stimulated the proliferation of ESCs. circ6401 13-21 microRNA 29b-1 Homo sapiens 43-52 32512188-0 2020 Epigallocatechin gallate reverses gastric cancer by regulating the long noncoding RNA LINC00511/miR-29b/KDM2A axis. epigallocatechin gallate 0-24 microRNA 29b-1 Homo sapiens 96-103 33174591-0 2020 Paper Withdrawn: Quercetin attenuates high glucose-induced injury in human retinal pigment epithelial cell line ARPE-19 by up-regulation of miR-29b. Quercetin 17-26 microRNA 29b-1 Homo sapiens 140-147 33174591-0 2020 Paper Withdrawn: Quercetin attenuates high glucose-induced injury in human retinal pigment epithelial cell line ARPE-19 by up-regulation of miR-29b. Glucose 43-50 microRNA 29b-1 Homo sapiens 140-147 33415004-0 2020 Molecular mechanisms underlying the enhancement of carbon ion beam radiosensitivity of osteosarcoma cells by miR-29b. Carbon 51-57 microRNA 29b-1 Homo sapiens 109-116 33415004-8 2020 When used in combination with miR-29b mimic, carbon ion beam markedly inhibited invasion, migration, and proliferation of OSA cells and promoted apoptosis by inhibiting AKT phosphorylation in a Sp1/PTEN-mediated manner. Carbon 45-51 microRNA 29b-1 Homo sapiens 30-37 33415004-9 2020 Taken together, miR-29b mimic improved the radiosensitivity of OSA cells via the PTEN-AKT-Sp1 signaling pathway, presenting a novel strategy for the development of carbon ion beam combination therapy. Carbon 164-170 microRNA 29b-1 Homo sapiens 16-23 33261656-0 2020 Circ6401, a novel circular RNA, is implicated in repair of the damaged endometrium by Wharton"s jelly-derived mesenchymal stem cells through regulation of the miR-29b-1-5p/RAP1B axis. circ6401 0-8 microRNA 29b-1 Homo sapiens 159-168 32358723-4 2020 Concerning that, the aim of this work was focused on the co-delivery of miR-29b and retinoic acid (RA) into NSCLC cells by multifunctional micellar nanosystems (Pluronic P123 or Pluronic P103 linked to polyethyleneimine (PEI)). aziridine 204-221 microRNA 29b-1 Homo sapiens 72-79 32358723-4 2020 Concerning that, the aim of this work was focused on the co-delivery of miR-29b and retinoic acid (RA) into NSCLC cells by multifunctional micellar nanosystems (Pluronic P123 or Pluronic P103 linked to polyethyleneimine (PEI)). pei 223-226 microRNA 29b-1 Homo sapiens 72-79 32790250-0 2020 Dihydroartemisinin/miR-29b combination therapy increases the pro-apoptotic effect of dihydroartemisinin on cholangiocarcinoma cell lines by regulating Mcl-1 expression. artenimol 85-103 microRNA 29b-1 Homo sapiens 19-26 32790250-2 2020 OBJECTIVES: To investigate the role of DHA and miR-29b on the proliferation and apoptosis of cholangiocarcinoma cells, and to explore whether DHA exerted its role through the miR-29b/Mcl-1 signaling pathway. artenimol 142-145 microRNA 29b-1 Homo sapiens 175-182 32790250-4 2020 The inhibitory effects of DHA and miR-29b on proliferation were detected using MTT assay. monooxyethylene trimethylolpropane tristearate 79-82 microRNA 29b-1 Homo sapiens 34-41 32790250-7 2020 RESULTS: The DHA increased miR-29b expression in HUCCT-1 and FRH201 cells. artenimol 13-16 microRNA 29b-1 Homo sapiens 27-34 32790250-8 2020 The MTT assay showed that DHA+miR-29b combination therapy promoted the inhibition effects on the proliferation of HUCCT-1 and FRH201 cells. monooxyethylene trimethylolpropane tristearate 4-7 microRNA 29b-1 Homo sapiens 30-37 32790250-12 2020 CONCLUSIONS: The DHA and miR-29b have a pro-apoptotic effect on cholangiocarcinoma cells through the DHA/miR-29b/Mcl-1 pathway, possibly by upregulating the expression of the pro-apoptotic protein Mcl-1S and thus increasing the proportion of Mcl-1S protein among the total amount of Mcl-1 protein. artenimol 17-20 microRNA 29b-1 Homo sapiens 105-112 32790250-12 2020 CONCLUSIONS: The DHA and miR-29b have a pro-apoptotic effect on cholangiocarcinoma cells through the DHA/miR-29b/Mcl-1 pathway, possibly by upregulating the expression of the pro-apoptotic protein Mcl-1S and thus increasing the proportion of Mcl-1S protein among the total amount of Mcl-1 protein. artenimol 101-104 microRNA 29b-1 Homo sapiens 25-32 32790250-12 2020 CONCLUSIONS: The DHA and miR-29b have a pro-apoptotic effect on cholangiocarcinoma cells through the DHA/miR-29b/Mcl-1 pathway, possibly by upregulating the expression of the pro-apoptotic protein Mcl-1S and thus increasing the proportion of Mcl-1S protein among the total amount of Mcl-1 protein. artenimol 101-104 microRNA 29b-1 Homo sapiens 105-112 32124130-8 2020 Dual-luciferase assay was employed to identify interaction between p53 and miR-29b in HTFs. htfs 86-90 microRNA 29b-1 Homo sapiens 75-82 32497630-8 2020 KEY FINDINGS: High glucose (HG) challenge led to increased circCOL1A2, VEGF, MMP-2, MMP-9 levels, but decreased miR-29b level in hRMECs. Glucose 19-26 microRNA 29b-1 Homo sapiens 112-119 32730124-0 2020 Triptolide protects human retinal pigment epithelial ARPE-19 cells against high glucose-induced cell injury by regulation of miR-29b/PTEN. triptolide 0-10 microRNA 29b-1 Homo sapiens 125-132 31960917-0 2020 Quercetin attenuates high glucose induced injury in human retinal pigment epithelial cell line ARPE-19 by up-regulation of miR-29b. Quercetin 0-9 microRNA 29b-1 Homo sapiens 123-130 32034483-6 2020 Then, dual luciferase assay supported the interaction of miR-29b-1 with LOC646329-variant D transcript. loc646329 72-81 microRNA 29b-1 Homo sapiens 57-66 32034483-12 2020 Data also indicated that LOC646329-variant D exerts its suppression effect on CRC progression through sponging miR-29b, which in turn regulates Wnt and TGFB signaling pathways. loc646329 25-34 microRNA 29b-1 Homo sapiens 111-118 31960917-0 2020 Quercetin attenuates high glucose induced injury in human retinal pigment epithelial cell line ARPE-19 by up-regulation of miR-29b. Glucose 26-33 microRNA 29b-1 Homo sapiens 123-130 31960917-5 2020 The association between quercetin and miR-29b expression as well as the downstream pathways was studied by qRT-PCR and western blot. Quercetin 24-33 microRNA 29b-1 Homo sapiens 38-45 31960917-8 2020 MiR-29b was low-expressed in high glucose-treated cell, but quercetin elevated its expression. Glucose 34-41 microRNA 29b-1 Homo sapiens 0-7 31960917-9 2020 Moreover, the protective action of quercetin towards ARPE-19 cells was attenuated when miR-29b was suppressed. Quercetin 35-44 microRNA 29b-1 Homo sapiens 87-94 31960917-10 2020 Also, quercetin promoted PTEN/AKT pathway while inhibited NF-kappaB pathway via a miR-29b-dependent way. Quercetin 6-15 microRNA 29b-1 Homo sapiens 82-89 31960917-12 2020 The protective action of quercetin may due to its regulation on miR-29b expression as well as PTEN/AKT and NF-kappaB pathways. Quercetin 25-34 microRNA 29b-1 Homo sapiens 64-71 31621972-6 2020 Overexpression of miR-29b markedly inhibited cell viability, promoted sensitivity to L-OHP, stimulated cell apoptosis (all p < .05), and decreased the levels of ABCG2 and p-gp in cancer cells, whereas suppression of miR-29b showed contrary results. oxaliplatin 85-90 microRNA 29b-1 Homo sapiens 18-25 31492208-3 2020 The lipofectaminebased miR-29b showed a typical concentration-dependent cytotoxic effect in the cancer cells. lipofectaminebased 4-22 microRNA 29b-1 Homo sapiens 23-30 31739067-0 2020 MiR-29b interacts with IFN-gamma and induces DNA hypomethylation in CD4+ T cells of oral lichen planus. planus 96-102 microRNA 29b-1 Homo sapiens 0-7 32210579-10 2020 Furthermore, we demonstrated that miR-29b could directly interact with HANR and abolished HANR-induced sorafenib resistance by suppressing autophagy in HepG2/sora and Huh7/sora cells. Sorafenib 103-112 microRNA 29b-1 Homo sapiens 34-41 32210579-11 2020 Moreover, ATG9A was validated as a target of miR-29b and its overexpression obviously reversed the inhibitory effect of miR-29b on sorafenib resistance and autophagy. Sorafenib 131-140 microRNA 29b-1 Homo sapiens 45-52 32210579-11 2020 Moreover, ATG9A was validated as a target of miR-29b and its overexpression obviously reversed the inhibitory effect of miR-29b on sorafenib resistance and autophagy. Sorafenib 131-140 microRNA 29b-1 Homo sapiens 120-127 32210579-14 2020 Conclusion: Our study revealed HANR enhanced sorafenib resistance by acting as an autophagy promoter by regulating miR-29b/ATG9A axis in sorafenib-resistant HCC cells and might provide potential therapeutic strategies for HCC treatment. Sorafenib 45-54 microRNA 29b-1 Homo sapiens 115-122 32210579-14 2020 Conclusion: Our study revealed HANR enhanced sorafenib resistance by acting as an autophagy promoter by regulating miR-29b/ATG9A axis in sorafenib-resistant HCC cells and might provide potential therapeutic strategies for HCC treatment. Sorafenib 137-146 microRNA 29b-1 Homo sapiens 115-122 32141561-10 2020 Moreover, our results showed that miR-29b expression in Temozolomide (TMZ)-resistance cell lines U251/TMZ and U87MG/TMZ was markedly lower than that of TMZ-sensitivity cell lines U251 and U87MG. Temozolomide 56-68 microRNA 29b-1 Homo sapiens 34-41 32141561-10 2020 Moreover, our results showed that miR-29b expression in Temozolomide (TMZ)-resistance cell lines U251/TMZ and U87MG/TMZ was markedly lower than that of TMZ-sensitivity cell lines U251 and U87MG. Temozolomide 70-73 microRNA 29b-1 Homo sapiens 34-41 32141561-10 2020 Moreover, our results showed that miR-29b expression in Temozolomide (TMZ)-resistance cell lines U251/TMZ and U87MG/TMZ was markedly lower than that of TMZ-sensitivity cell lines U251 and U87MG. Temozolomide 102-105 microRNA 29b-1 Homo sapiens 34-41 32141561-16 2020 As expected, the effect of miR-29b upregulation on cell growth and apoptosis of TMZ-resistant glioma cells was reversed by STAT3 overexpression. Temozolomide 80-83 microRNA 29b-1 Homo sapiens 27-34 32141561-18 2020 CONCLUSIONS: MiR-29b enhances the cell sensitivity to TMZ by inhibiting STAT3 in glioma. Temozolomide 54-57 microRNA 29b-1 Homo sapiens 13-20 32210579-0 2020 HANR Enhances Autophagy-Associated Sorafenib Resistance Through miR-29b/ATG9A Axis in Hepatocellular Carcinoma. Sorafenib 35-44 microRNA 29b-1 Homo sapiens 64-71 32020216-9 2020 Notably, miR-29b was found to be reversely expressed compared to TET1 in curcumin- and 5"-aza-CdR-treated cells, suggesting its involvement in the regulation of TET1. Curcumin 73-81 microRNA 29b-1 Homo sapiens 9-16 31313842-2 2020 We show that NRF2 activation stimulates cell growth and markedly reduces reactive oxygen species (ROS) generation, whereas miR-29b-1-5p overexpression increases ROS generation and reduces cell proliferation. Reactive Oxygen Species 161-164 microRNA 29b-1 Homo sapiens 123-132 31313842-6 2020 We also show that parthenolide, a naturally occurring small molecule, induces the expression of miR-29b-1-5p which could suppress NRF2 activation via AKT inhibition. parthenolide 18-30 microRNA 29b-1 Homo sapiens 96-105 31621972-9 2020 Taken together, our study suggests that miR-29b inhibits cell growth and promotes sensitivity to L-OHP in colon cancer by targeting FOLR1. oxaliplatin 97-102 microRNA 29b-1 Homo sapiens 40-47 31737629-7 2019 We found that positive modulation of miR29b and inhibition of H19 and VEGFA significantly attenuates high glucose-induced endothelial inflammation and oxidative stress. Glucose 106-113 microRNA 29b-1 Homo sapiens 37-43 31418997-0 2019 Long noncoding RNA XIST enhances ethanol-induced hepatic stellate cells autophagy and activation via miR-29b/HMGB1 axis. Ethanol 33-40 microRNA 29b-1 Homo sapiens 101-108 31418997-10 2019 Furthermore, XIST served as a competitive endogenous RNA of miR-29b to facilitate HMGB1 expression, and thus enhanced ethanol-induced HSCs autophagy and activation. Ethanol 118-125 microRNA 29b-1 Homo sapiens 60-67 31418997-12 2019 Collectively, XIST enhances ethanol-induced HSCs autophagy and activation via miR-29b/HMGB1 axis. Ethanol 28-35 microRNA 29b-1 Homo sapiens 78-85 31029553-5 2019 Mechanistically, we reveal a novel function of miR-29b in regulating intracellular reactive oxygen species signaling and explore a potential application for its use in combination with therapies known to increase oxidative stress such as radiation. Reactive Oxygen Species 83-106 microRNA 29b-1 Homo sapiens 47-54 31508952-8 2019 Interestingly, PFOS (10 muM) significantly increased miR29-b (p < 0.01), which has been previously reported to be associated with PE. perfluorooctane sulfonic acid 15-19 microRNA 29b-1 Homo sapiens 53-60 31508952-9 2019 The observed epigenetic effects were shown to be dependent on the expression of miR-29b, as knockdown of miR-29b significantly alters the gene and protein expression of DNMT1, DNMT3A, DNMT3B, SIRT1, and SIRT3 and ROS production as well as global DNA methylation and protein acetylation. Reactive Oxygen Species 213-216 microRNA 29b-1 Homo sapiens 80-87 31508952-9 2019 The observed epigenetic effects were shown to be dependent on the expression of miR-29b, as knockdown of miR-29b significantly alters the gene and protein expression of DNMT1, DNMT3A, DNMT3B, SIRT1, and SIRT3 and ROS production as well as global DNA methylation and protein acetylation. Reactive Oxygen Species 213-216 microRNA 29b-1 Homo sapiens 105-112 31646594-15 2019 CONCLUSIONS: Propofol inhibited cell proliferation, migration and invasion by upregulating miR-29a, miR-29b and miR-29c and downregulating MMP-2. Propofol 13-21 microRNA 29b-1 Homo sapiens 100-107 31029553-6 2019 Moreover, miR-29b inhibits DNA damage repair by targeting phosphate and tension homology deleted on chromsome ten (PTEN), and overexpression of PTEN could partially rescue miR-29b-mediated homologous recombination (HR)-DNA damage repair and increase radiosensitivity. Phosphates 58-67 microRNA 29b-1 Homo sapiens 10-17 31029553-6 2019 Moreover, miR-29b inhibits DNA damage repair by targeting phosphate and tension homology deleted on chromsome ten (PTEN), and overexpression of PTEN could partially rescue miR-29b-mediated homologous recombination (HR)-DNA damage repair and increase radiosensitivity. Phosphates 58-67 microRNA 29b-1 Homo sapiens 172-179 30967527-0 2019 Bortezomib-inducible long non-coding RNA myocardial infarction associated transcript is an oncogene in multiple myeloma that suppresses miR-29b. Bortezomib 0-10 microRNA 29b-1 Homo sapiens 136-143 30742923-0 2019 Circular RNA circPTK2 regulates oxygen-glucose deprivation-activated microglia-induced hippocampal neuronal apoptosis via miR-29b-SOCS-1-JAK2/STAT3-IL-1beta signaling. oxygen-glucose 32-46 microRNA 29b-1 Homo sapiens 122-129 30896849-0 2019 Astaxanthin inhibits proliferation and induces apoptosis of LX-2 cells by regulating the miR-29b/Bcl-2 pathway. astaxanthine 0-11 microRNA 29b-1 Homo sapiens 89-96 30896849-6 2019 Additionally, Annexin V-fluorescein isothiocyanate/propidium iodide double staining and flow cytometry were used to evaluate the cell apoptosis, and overexpression of miR-29b increased cell apoptosis rates in AST-treated LX-2 cells; however, silencing of it had the opposite effect. Propidium 51-67 microRNA 29b-1 Homo sapiens 167-174 31111046-5 2019 The results showed that R9-LK15 maintained the stability of miR-29b in serum for up to 24 h. Moreover, R9-LK15 efficiently delivered miR-29b into BMSCs; the transfection efficiency was ~10-fold higher than that achieved using Lipofectamine 2000. Lipofectamine 226-244 microRNA 29b-1 Homo sapiens 133-140 30652495-12 2019 The antioxidant N-acetylcysteine prevents CSE-induced miR-29b downregulation and BRD4 and IL-8 upregulation. Acetylcysteine 16-32 microRNA 29b-1 Homo sapiens 54-61 30518744-8 2018 RESULTS miR-29a, miR-29b, and miR-29c were significantly downregulated in MG-63/MTX and U2OS/MTX cells and in chemotherapy poor-response osteosarcoma tissues. Magnesium 74-76 microRNA 29b-1 Homo sapiens 17-24 30756471-8 2019 Additionally, age, serum triglyceride and fasting plasma glucose (FPG) levels were independently associated with miR-29b (beta +- standard error [SE] = 0.004 +- 0.002, P = 0.019 for age; beta +- SE = 0.110 +- 0.054, P = 0.042 for triglyceride; and beta +- SE = 0.389 +- 0.161, P = 0.016 for FPG). Triglycerides 25-37 microRNA 29b-1 Homo sapiens 113-120 30756471-8 2019 Additionally, age, serum triglyceride and fasting plasma glucose (FPG) levels were independently associated with miR-29b (beta +- standard error [SE] = 0.004 +- 0.002, P = 0.019 for age; beta +- SE = 0.110 +- 0.054, P = 0.042 for triglyceride; and beta +- SE = 0.389 +- 0.161, P = 0.016 for FPG). Glucose 57-64 microRNA 29b-1 Homo sapiens 113-120 30756471-8 2019 Additionally, age, serum triglyceride and fasting plasma glucose (FPG) levels were independently associated with miR-29b (beta +- standard error [SE] = 0.004 +- 0.002, P = 0.019 for age; beta +- SE = 0.110 +- 0.054, P = 0.042 for triglyceride; and beta +- SE = 0.389 +- 0.161, P = 0.016 for FPG). Triglycerides 230-242 microRNA 29b-1 Homo sapiens 113-120 30915884-0 2019 The role of lncRNA MSC-AS1/miR-29b-3p axis-mediated CDK14 modulation in pancreatic cancer proliferation and Gemcitabine-induced apoptosis. gemcitabine 108-119 microRNA 29b-1 Homo sapiens 27-34 30518744-8 2018 RESULTS miR-29a, miR-29b, and miR-29c were significantly downregulated in MG-63/MTX and U2OS/MTX cells and in chemotherapy poor-response osteosarcoma tissues. Methotrexate 80-83 microRNA 29b-1 Homo sapiens 17-24 30518744-8 2018 RESULTS miR-29a, miR-29b, and miR-29c were significantly downregulated in MG-63/MTX and U2OS/MTX cells and in chemotherapy poor-response osteosarcoma tissues. Methotrexate 93-96 microRNA 29b-1 Homo sapiens 17-24 29619741-5 2018 In our recently published study, we have identified a set of miRNAs including miR-145 and miR-29b families differentially expressed in SH-SY5Y cells exposed sequentially with retinoic acid + brain-derived neurotrophic factor (RA+BDNF) for differentiation into mature neurons (Mol Neurobiol (2016) doi: https://doi.org/10.1007/s12035-016-0042-9 ). Tretinoin 175-188 microRNA 29b-1 Homo sapiens 90-97 29374012-5 2018 The mutation of Mir29b-1/a gene led to preferential differential expression of genes related to nitric oxide including Lypla1. Nitric Oxide 96-108 microRNA 29b-1 Homo sapiens 16-24 30006350-9 2018 Targeted proteomic analysis of affinity-purified samples identified several proteins interacting with synthetic oligonucleotides mimicking miR-29b, but these proteins did not interact with miR-29a. Oligonucleotides 112-128 microRNA 29b-1 Homo sapiens 139-146 30006350-10 2018 One of these proteins, ADP/ATP translocase 2 (ANT2), known to be involved in mitotic spindle formation, colocalized with miR-29b in perinuclear clusters independently of Argonaute 2. Adenosine Diphosphate 23-26 microRNA 29b-1 Homo sapiens 121-128 30006350-10 2018 One of these proteins, ADP/ATP translocase 2 (ANT2), known to be involved in mitotic spindle formation, colocalized with miR-29b in perinuclear clusters independently of Argonaute 2. Adenosine Triphosphate 27-30 microRNA 29b-1 Homo sapiens 121-128 30006350-12 2018 Our findings reveal that miR-29 regulates nuclear morphology during mitosis and that this critical function is unique to the miR-29b isoform. mir-29 25-31 microRNA 29b-1 Homo sapiens 125-132 29896234-0 2018 Inhibition of prostaglandin E2 protects abdominal aortic aneurysm from expansion through regulating miR-29b-mediated fibrotic ECM expression. Dinoprostone 14-30 microRNA 29b-1 Homo sapiens 100-107 29896234-4 2018 Herein we found that miR-29b was upregulated in aortic smooth muscle cells upon prostaglandin E2 (PGE2) stimulation whereas indomethacin treatment downregulated miR-29b expression. Dinoprostone 80-96 microRNA 29b-1 Homo sapiens 21-28 29896234-4 2018 Herein we found that miR-29b was upregulated in aortic smooth muscle cells upon prostaglandin E2 (PGE2) stimulation whereas indomethacin treatment downregulated miR-29b expression. Dinoprostone 98-102 microRNA 29b-1 Homo sapiens 21-28 29896234-4 2018 Herein we found that miR-29b was upregulated in aortic smooth muscle cells upon prostaglandin E2 (PGE2) stimulation whereas indomethacin treatment downregulated miR-29b expression. Indomethacin 124-136 microRNA 29b-1 Homo sapiens 161-168 29896234-8 2018 In aggregate, our study suggests that PGE2 may accelerate ECM degradation through decreasing miR-29b expression. Dinoprostone 38-42 microRNA 29b-1 Homo sapiens 93-100 29246928-0 2018 Identification of miR-29b targets using 3-cyanovinylcarbazole containing mimics. 3-Cyanovinylcarbazole 40-61 microRNA 29b-1 Homo sapiens 18-25 29246928-4 2018 Here, we describe a novel method to identify microRNA targets using miR-29b mimics containing 3-cyanovinylcarbazole (CNVK), a photolabile nucleoside analog. 3-Cyanovinylcarbazole 94-115 microRNA 29b-1 Homo sapiens 68-75 29246928-4 2018 Here, we describe a novel method to identify microRNA targets using miR-29b mimics containing 3-cyanovinylcarbazole (CNVK), a photolabile nucleoside analog. Nucleosides 138-148 microRNA 29b-1 Homo sapiens 68-75 29246928-5 2018 We demonstrate that biotin-tagged, CNVK-containing miR-29b (CNVK-miR-29b) mimics are nontoxic in cell culture, associate with endogenous mammalian Argonaute2, are sensitive for known targets and recapitulate endogenous transcript destabilization. Biotin 20-26 microRNA 29b-1 Homo sapiens 51-58 29246928-5 2018 We demonstrate that biotin-tagged, CNVK-containing miR-29b (CNVK-miR-29b) mimics are nontoxic in cell culture, associate with endogenous mammalian Argonaute2, are sensitive for known targets and recapitulate endogenous transcript destabilization. Biotin 20-26 microRNA 29b-1 Homo sapiens 65-72 30377134-6 2018 Compared with the blank vector, the lentiviral vector LV-hsa-miR-29b caused significantly increased expression of miR-29b in QBC939 cells (P &lt; 0.01), which exhibited suppressed cell proliferation and clone formation (P &lt; 0.01 or 0.05), cell cycle arrest at the S phase (P &lt; 0.05), and significantly increased cell apoptosis (P &lt; 0.01). Adenosine Monophosphate 142-145 microRNA 29b-1 Homo sapiens 61-68 30377134-6 2018 Compared with the blank vector, the lentiviral vector LV-hsa-miR-29b caused significantly increased expression of miR-29b in QBC939 cells (P &lt; 0.01), which exhibited suppressed cell proliferation and clone formation (P &lt; 0.01 or 0.05), cell cycle arrest at the S phase (P &lt; 0.05), and significantly increased cell apoptosis (P &lt; 0.01). Adenosine Monophosphate 142-145 microRNA 29b-1 Homo sapiens 114-121 30377134-6 2018 Compared with the blank vector, the lentiviral vector LV-hsa-miR-29b caused significantly increased expression of miR-29b in QBC939 cells (P &lt; 0.01), which exhibited suppressed cell proliferation and clone formation (P &lt; 0.01 or 0.05), cell cycle arrest at the S phase (P &lt; 0.05), and significantly increased cell apoptosis (P &lt; 0.01). Adenosine Monophosphate 227-230 microRNA 29b-1 Homo sapiens 61-68 30377134-6 2018 Compared with the blank vector, the lentiviral vector LV-hsa-miR-29b caused significantly increased expression of miR-29b in QBC939 cells (P &lt; 0.01), which exhibited suppressed cell proliferation and clone formation (P &lt; 0.01 or 0.05), cell cycle arrest at the S phase (P &lt; 0.05), and significantly increased cell apoptosis (P &lt; 0.01). Adenosine Monophosphate 227-230 microRNA 29b-1 Homo sapiens 114-121 30092402-5 2018 Injection of sCA-miR-29a-3p or sCA-miR-29b-3p into mouse tail veins markedly prevented and restored inflammation because of dextran sulfate sodium (DSS)-induced colitis. Dextran Sulfate 124-146 microRNA 29b-1 Homo sapiens 35-42 30092402-5 2018 Injection of sCA-miR-29a-3p or sCA-miR-29b-3p into mouse tail veins markedly prevented and restored inflammation because of dextran sulfate sodium (DSS)-induced colitis. Dextran Sulfate 148-151 microRNA 29b-1 Homo sapiens 35-42 29884225-0 2018 CircIBTK inhibits DNA demethylation and activation of AKT signaling pathway via miR-29b in peripheral blood mononuclear cells in systemic lupus erythematosus. circibtk 0-8 microRNA 29b-1 Homo sapiens 80-87 29532991-1 2018 It has been recently demonstrated that high pre-treatment levels of miR-29b positively correlated with the response of patients with acute myeloid leukaemia (AML) to hypomethylating agents. hypomethylating agents 166-188 microRNA 29b-1 Homo sapiens 68-75 28858294-6 2018 We also found that C6 ceramide (5-20 mumol/L) dose-dependently stimulated exosome secretion and increased exosomal levels of tumor-suppressive miRs (miR 202, miR 16, miR 29b and miR 15a). N-caproylsphingosine 19-30 microRNA 29b-1 Homo sapiens 166-173 28528141-13 2018 Although the OIM or PC treatment upregulated miR-21, miR-29b, and miR-146a, only miR-146a was able to be induced by PC in combination with OIM. pc 20-22 microRNA 29b-1 Homo sapiens 53-60 29398368-10 2018 Besides, miR-29b antagomir induced decrease of TNF-alpha, ROS production and NADPH oxidase activity and down-regulated the expression of p-ERK and p-p38 in the presence of oxLDL. Reactive Oxygen Species 58-61 microRNA 29b-1 Homo sapiens 9-16 29195902-10 2018 Dickkopf-1 protein, the Wnt/beta-catenin signaling inhibitor, suppressed anti-miR-29b-enhanced HASMCs calcification. hasmcs 95-101 microRNA 29b-1 Homo sapiens 78-85 28988362-9 2018 In the presence of MMP-2 inhibitor SB-3CT, the cell viability and apoptosis of SMC cells were significantly reduced and enhanced, respectively, while the miR-29b -inhibited cell viability and -induced cell apoptosis were not significantly changed. SB 3CT compound 35-41 microRNA 29b-1 Homo sapiens 154-161 29440967-6 2018 Methods: PCa DU145 and PC-3 cells were transfected with 100 muL of OPTI-MEM I containing 100 nmol of miR-29b (or its inhibitor) along with 1.5 muL of lipofectamine. opti-mem i 67-77 microRNA 29b-1 Homo sapiens 101-108 29117536-7 2018 Inhibition of miR-29b-1-5p attenuated cardiomyocyte apoptosis upon hydrogen peroxide treatment. Hydrogen Peroxide 67-84 microRNA 29b-1 Homo sapiens 14-23 29087603-0 2018 MiR-29b expression is associated with a dexmedetomidine-mediated protective effect against oxygen-glucose deprivation-induced injury to SK-N-SH cells in vitro. Dexmedetomidine 40-55 microRNA 29b-1 Homo sapiens 0-7 29087603-0 2018 MiR-29b expression is associated with a dexmedetomidine-mediated protective effect against oxygen-glucose deprivation-induced injury to SK-N-SH cells in vitro. oxygen-glucose 91-105 microRNA 29b-1 Homo sapiens 0-7 29087603-6 2018 Next, the association of miR-29b with the protective effect of Dex against ischemic brain injury was studied through the enhancement or inhibition of miR-29b expression by transfection with an miR-29b mimic or inhibitor. Dexmedetomidine 63-66 microRNA 29b-1 Homo sapiens 25-32 29087603-7 2018 We demonstrated that Dex treatment could reduce miR-29b expression, increase cell viability, and inhibit cell apoptosis in the OGD-induced neuronal injury model in vitro. Dexmedetomidine 21-24 microRNA 29b-1 Homo sapiens 48-55 29087603-9 2018 Moreover, up-regulation of miR-29b reversed the protective effect of Dex treatment against OGD-induced neuronal injury. Dexmedetomidine 69-72 microRNA 29b-1 Homo sapiens 27-34 29087603-11 2018 Elucidation of the role played by miR-29b in ischemia, and identification of a definite association between Dex and miR-29b may lead to the development of new strategies for treating ischemic brain injuries. Dexmedetomidine 108-111 microRNA 29b-1 Homo sapiens 116-123 29552311-0 2018 MiR-29b reverses oxaliplatin-resistance in colorectal cancer by targeting SIRT1. Oxaliplatin 17-28 microRNA 29b-1 Homo sapiens 0-7 29552311-4 2018 We found that intracellular expression of miR-29b was decreased when the SW480 cells became oxaliplatin-resistant. Oxaliplatin 92-103 microRNA 29b-1 Homo sapiens 42-49 29552311-5 2018 More importantly, overexpression of miR-29b resensitized OR-SW480 cells to oxaliplatin treatment. Oxaliplatin 75-86 microRNA 29b-1 Homo sapiens 36-43 29552311-7 2018 Overexpression of miR-29b in oxaliplatin-treated OR-SW480 decreased the expression of SIRT1 to enhance the ROS production and JNK phosphorylation, and thus promoting apoptosis via activation of caspase 9, 7 and 3. Oxaliplatin 29-40 microRNA 29b-1 Homo sapiens 18-25 29552311-7 2018 Overexpression of miR-29b in oxaliplatin-treated OR-SW480 decreased the expression of SIRT1 to enhance the ROS production and JNK phosphorylation, and thus promoting apoptosis via activation of caspase 9, 7 and 3. ros 107-110 microRNA 29b-1 Homo sapiens 18-25 29552311-8 2018 On the other hand, expression plasmid of SIRT1, N-acetyl cysteine or SP600125 (JNK specific inhibitor) abolished the effect of miR-29b on oxaliplatin-treated OR-SW480. Acetylcysteine 48-65 microRNA 29b-1 Homo sapiens 127-134 29552311-8 2018 On the other hand, expression plasmid of SIRT1, N-acetyl cysteine or SP600125 (JNK specific inhibitor) abolished the effect of miR-29b on oxaliplatin-treated OR-SW480. pyrazolanthrone 69-77 microRNA 29b-1 Homo sapiens 127-134 29552311-8 2018 On the other hand, expression plasmid of SIRT1, N-acetyl cysteine or SP600125 (JNK specific inhibitor) abolished the effect of miR-29b on oxaliplatin-treated OR-SW480. Oxaliplatin 138-149 microRNA 29b-1 Homo sapiens 127-134 29552311-9 2018 We therefore demonstrated that miR-29b reverses oxaliplatin-resistance in colorectal cancer by targeting SIRT1/ROS/JNK pathway. Oxaliplatin 48-59 microRNA 29b-1 Homo sapiens 31-38 29552311-9 2018 We therefore demonstrated that miR-29b reverses oxaliplatin-resistance in colorectal cancer by targeting SIRT1/ROS/JNK pathway. ros 111-114 microRNA 29b-1 Homo sapiens 31-38 29221174-3 2017 Low expression of miR-29b was significantly associated with DNA methylation, and treatment with DNA methyltransferase inhibitor 5-Aza-20-deoxycytidine upregulated miR-29b in gastric cancer cells. 5-aza-20-deoxycytidine 128-150 microRNA 29b-1 Homo sapiens 18-25 29221174-3 2017 Low expression of miR-29b was significantly associated with DNA methylation, and treatment with DNA methyltransferase inhibitor 5-Aza-20-deoxycytidine upregulated miR-29b in gastric cancer cells. 5-aza-20-deoxycytidine 128-150 microRNA 29b-1 Homo sapiens 163-170 28465475-3 2017 MiR-29b is one of the significant down-regulated miRNAs in CAFs from the miRNA screening. cafs 59-63 microRNA 29b-1 Homo sapiens 0-7 30090550-6 2017 The results demonstrated that the supernatants from silica-treated macrophages not only caused the proliferation of fibroblasts (NIH-3T3 and MRC-5) but were also involved in the down-regulation of miR-29b. Silicon Dioxide 52-58 microRNA 29b-1 Homo sapiens 197-204 30090550-9 2017 These findings indicate that miR-29b inhibits the supernatants from silica-treated macrophages from inducing extracellular matrix synthesis, thus miR-29b might have a strong anti-fibrotic capacity in silicosis and serve as a potential therapeutic agent for the treatment. Silicon Dioxide 68-74 microRNA 29b-1 Homo sapiens 29-36 30090550-9 2017 These findings indicate that miR-29b inhibits the supernatants from silica-treated macrophages from inducing extracellular matrix synthesis, thus miR-29b might have a strong anti-fibrotic capacity in silicosis and serve as a potential therapeutic agent for the treatment. Silicon Dioxide 68-74 microRNA 29b-1 Homo sapiens 146-153 28431975-10 2017 The results showed that lower expressed miR-29b-1-5p decreased the IC50 of MCF-7/Adr cells and higher expressed miR-29b-1-5p, weaken the effects of liposomal curcumin to Adr-resistance. Curcumin 158-166 microRNA 29b-1 Homo sapiens 40-49 28431975-10 2017 The results showed that lower expressed miR-29b-1-5p decreased the IC50 of MCF-7/Adr cells and higher expressed miR-29b-1-5p, weaken the effects of liposomal curcumin to Adr-resistance. Curcumin 158-166 microRNA 29b-1 Homo sapiens 112-121 28701793-3 2017 However, miR-29b-1/a overexpression significantly repressed TAM-resistant LCC9 cell proliferation, suggesting that miR-29b-1/a is not mediating TAM resistance but acts as a tumor suppressor in TAM-resistant cells. Tamoxifen 60-63 microRNA 29b-1 Homo sapiens 9-18 28701793-3 2017 However, miR-29b-1/a overexpression significantly repressed TAM-resistant LCC9 cell proliferation, suggesting that miR-29b-1/a is not mediating TAM resistance but acts as a tumor suppressor in TAM-resistant cells. Tamoxifen 60-63 microRNA 29b-1 Homo sapiens 115-124 28701793-8 2017 LCC9-sepecific miR-29b-1/a-regulated GO processes include oxidative phosphorylation, ATP metabolism, and apoptosis. Adenosine Triphosphate 85-88 microRNA 29b-1 Homo sapiens 15-24 28886082-12 2017 The expression of miR-29b that is known to putatively regulate the global methylation by modulating the expression of epigenetic modifiers was observed to be down regulated by haloperidol. Haloperidol 176-187 microRNA 29b-1 Homo sapiens 18-25 28886082-13 2017 In addition to miR-29b, miR-22 was also found to be downregulated by haloperidol treatment. Haloperidol 69-80 microRNA 29b-1 Homo sapiens 15-22 28919708-11 2017 AOS treatment reduced the levels of miR-29b, TLR4, mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF-kappa B), interleukin 1 (IL-1) beta, and interleukin 6 (IL-6). D-(+)-ALLOSE 0-3 microRNA 29b-1 Homo sapiens 36-43 28423357-4 2017 Cell proliferation was evaluated by cell counting kit (CCK8) and 5-Ethynyl-2"- deoxyuridine (EdU) and cell apoptosis was assayed with flow cytometry assay (FCA), which indicated miR-29b can inhibit the proliferation and promote the apoptosis of glioma cells. 5-ethynyl-2'-deoxyuridine 65-91 microRNA 29b-1 Homo sapiens 178-185 28465475-4 2017 The role of miR-29b in the interaction between CAFs and breast cancer is still unclear. cafs 47-51 microRNA 29b-1 Homo sapiens 12-19 28465475-5 2017 In the present study, we investigated the effects of CAFs on breast cancer cell proliferation and metastasis regulated by miR-29b. cafs 53-57 microRNA 29b-1 Homo sapiens 122-129 28465475-8 2017 We also found that the expression of CCL11 and CXCL14 could be regulated by miR-29b in CAFs. cafs 87-91 microRNA 29b-1 Homo sapiens 76-83 28465475-9 2017 Our results illustrate that down-regulation of miR-29b in CAFs plays an important role in tumor stroma by activating p38-STAT1 in breast cancer cells. cafs 58-62 microRNA 29b-1 Homo sapiens 47-54 28377429-10 2017 Plasma miR-29b and -499 are acutely elevated post-AC, with dose response relationships observed with anthracycline dose and markers of cardiac injury. Anthracyclines 101-114 microRNA 29b-1 Homo sapiens 7-14 28423652-3 2017 We found that miR-29b-1-5p was downregulated in human TNBC tissues and cell lines. CHEMBL3740941 24-26 microRNA 29b-1 Homo sapiens 14-23 28185889-5 2017 We show that miR-29b significantly increases etoposide toxicity in HeLa cells. Etoposide 45-54 microRNA 29b-1 Homo sapiens 13-20 28185889-7 2017 Despite downregulation of Mcl-1 by all three miR-29 family members, only miR-29b significantly enhanced etoposide toxicity. Etoposide 104-113 microRNA 29b-1 Homo sapiens 73-80 28185889-11 2017 In conclusion, we show that miR-29b has the synergistic effect with etoposide treatment in the HeLa cells and that this effect is linked to Mcl-1 protein expression and nuclear shuttling of miR-29b. Etoposide 68-77 microRNA 29b-1 Homo sapiens 28-35 28185889-11 2017 In conclusion, we show that miR-29b has the synergistic effect with etoposide treatment in the HeLa cells and that this effect is linked to Mcl-1 protein expression and nuclear shuttling of miR-29b. Etoposide 68-77 microRNA 29b-1 Homo sapiens 190-197 28061433-4 2017 METHODS AND RESULTS: Lovastatin time/dose-dependently increased miR-29b expression and decreased proteasome activity in cultured human umbilical vein endothelial cells (HUVECs). Lovastatin 21-31 microRNA 29b-1 Homo sapiens 64-71 27986463-0 2017 Tamoxifen differentially regulates miR-29b-1 and miR-29a expression depending on endocrine-sensitivity in breast cancer cells. Tamoxifen 0-9 microRNA 29b-1 Homo sapiens 35-44 27986463-9 2017 These results suggest miR-29b-1/a has tumor suppressor activity in TAM-resistant cells and does not appear to play a role in mediating TAM resistance. Tamoxifen 67-70 microRNA 29b-1 Homo sapiens 22-31 28122338-3 2017 In this study, we found a cohort of miRNAs were dysregulated upon treatment with cisplatin, among of which miR-29b was the most upregulated one. Cisplatin 81-90 microRNA 29b-1 Homo sapiens 107-114 28122338-5 2017 However, upon treatment with cisplatin, the expression of miR-29b was significantly up-regulated. Cisplatin 29-38 microRNA 29b-1 Homo sapiens 58-65 28122338-7 2017 While, inhibition of miR-29b could prevent the cisplatin-induced epithelial features, cell movement and angiogenesis of CC cells, which means miR-29b/STAT3 axis participates in the chemotherapy of cisplatin in CC. Cisplatin 47-56 microRNA 29b-1 Homo sapiens 21-28 28122338-7 2017 While, inhibition of miR-29b could prevent the cisplatin-induced epithelial features, cell movement and angiogenesis of CC cells, which means miR-29b/STAT3 axis participates in the chemotherapy of cisplatin in CC. Cisplatin 47-56 microRNA 29b-1 Homo sapiens 142-149 28122338-7 2017 While, inhibition of miR-29b could prevent the cisplatin-induced epithelial features, cell movement and angiogenesis of CC cells, which means miR-29b/STAT3 axis participates in the chemotherapy of cisplatin in CC. Cisplatin 197-206 microRNA 29b-1 Homo sapiens 21-28 28122338-7 2017 While, inhibition of miR-29b could prevent the cisplatin-induced epithelial features, cell movement and angiogenesis of CC cells, which means miR-29b/STAT3 axis participates in the chemotherapy of cisplatin in CC. Cisplatin 197-206 microRNA 29b-1 Homo sapiens 142-149 28061433-5 2017 Anti-miR-29b or overexpression of PA200 abolished lovastatin-induced inhibition of proteasome activity in HUVECs. Lovastatin 50-60 microRNA 29b-1 Homo sapiens 5-12 28061433-6 2017 In contrast, pre-miR-29b or PA200 siRNA mimics these effects of lovastatin on proteasome activity. Lovastatin 64-74 microRNA 29b-1 Homo sapiens 17-24 28061433-7 2017 Lovastatin inhibited oxidative stress induced by multiple oxidants including ox-LDL, H2O2, TNFalpha, homocysteine thiolactone (HTL), and high glucose (HG), which were reversed by inhibition of miR-29b in HUVECs. Lovastatin 0-10 microRNA 29b-1 Homo sapiens 193-200 28061433-9 2017 In vivo analysis revealed that administration of lovastatin remarkably suppressed oxidative stress and prevented endothelial dysfunction in rats with hyperglycemia, dyslipidemia, and hyperhomocysteinemia, as well as increased miR-29b expressions, reduced PA200 protein levels, and suppression of proteasome activity in aortic tissues. Lovastatin 49-59 microRNA 29b-1 Homo sapiens 226-233 28061433-10 2017 CONCLUSION: Upregulation of miR-29b expression is a common mechanism contributing to endothelial dysfunction induced by multiple cardiovascular risk factors through PA200-dependent proteasome-mediated oxidative stress, which is prevented by lovastatin. Lovastatin 241-251 microRNA 29b-1 Homo sapiens 28-35 27766427-6 2017 Our results showed that methylation levels of miR-29b promoter were significantly decreased in BVDV NADL-infected MDBK cells. nadl 100-104 microRNA 29b-1 Homo sapiens 46-53 27932253-5 2017 Arsenic increased the expression of miR-29b in white adipose tissue, as well as human mesenchymal stem cells (hMSCs) isolated from adipose tissue. Arsenic 0-7 microRNA 29b-1 Homo sapiens 36-43 27932253-6 2017 Exposing hMSCs to arsenic increased abundance of miR-29b and cyclin D1 to promote proliferation over differentiation. Arsenic 18-25 microRNA 29b-1 Homo sapiens 49-56 27932253-7 2017 Paradoxically, inhibition of miR-29b enhanced the inhibitory effect of arsenic on differentiation. Arsenic 71-78 microRNA 29b-1 Homo sapiens 29-36 27932253-9 2017 Temporal regulation of cyclin D1 is critical for adipogenic differentiation, and the data suggest a paradigm where arsenic disruption of miR-29b regulatory pathways impairs adipogenic differentiation and ultimately adipose metabolic homeostasis. Arsenic 115-122 microRNA 29b-1 Homo sapiens 137-144 26776158-10 2016 Moreover, inhibition of MAPK signaling by gefitinib led to decreased ETS1 and miR-29b expression with a corresponding increase in TET1 expression and increase in 5-hmC. Gefitinib 42-51 microRNA 29b-1 Homo sapiens 78-85 29050034-4 2017 Change in miR-29b was detected in EOC cells incubated in H2O2 culture by q-PCR. Hydrogen Peroxide 57-61 microRNA 29b-1 Homo sapiens 10-17 29050034-5 2017 Relative ROS levels were also detected in different EOC cultures, including modified miR-29b and SIRT1 levels as well as H2O2 incubation. Reactive Oxygen Species 9-12 microRNA 29b-1 Homo sapiens 85-92 28222438-10 2017 Additionally, miR-29b expression was reduced in the LNA-miR-29b inhibitors + PD98059 and LNA-miR-29b inhibitors + wortmannin groups. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 77-84 microRNA 29b-1 Homo sapiens 14-21 28222438-10 2017 Additionally, miR-29b expression was reduced in the LNA-miR-29b inhibitors + PD98059 and LNA-miR-29b inhibitors + wortmannin groups. Wortmannin 114-124 microRNA 29b-1 Homo sapiens 14-21 29050034-9 2017 H2O2 downregulated miR-29b in a time and dose-dependent manner. Hydrogen Peroxide 0-4 microRNA 29b-1 Homo sapiens 19-26 29050034-10 2017 miR-29b expression negatively correlated with ROS levels, whereas SIRT1 significantly stimulated ROS formation. Reactive Oxygen Species 46-49 microRNA 29b-1 Homo sapiens 0-7 29050034-14 2017 CONCLUSION: Together, our findings indicated that the miR-29b/SIRT1 axis has a protective effect against H2O2-induced damage of cell viability and oxidative stress and may provide novel options for miR-29b-based therapeutic approaches for EOC treatment. Hydrogen Peroxide 105-109 microRNA 29b-1 Homo sapiens 54-61 29050034-14 2017 CONCLUSION: Together, our findings indicated that the miR-29b/SIRT1 axis has a protective effect against H2O2-induced damage of cell viability and oxidative stress and may provide novel options for miR-29b-based therapeutic approaches for EOC treatment. Hydrogen Peroxide 105-109 microRNA 29b-1 Homo sapiens 198-205 27854545-0 2016 miR-29b Targets LPL and TDG Genes and Regulates Apoptosis and Triglyceride Production in MECs. Triglycerides 62-74 microRNA 29b-1 Homo sapiens 0-7 27854545-7 2016 Finally, miR-29b promoted triglyceride production and suppressed apoptosis in MECs, which might be attributed to the expressions of target genes LPL and TDG. Triglycerides 26-38 microRNA 29b-1 Homo sapiens 9-16 27430753-4 2016 The present study aimed to investigate the effects of paeoniflorin on the proliferation and apoptosis of SKO-007 MM cells, via its effects on the regulation of matrix metalloproteinase-2 (MMP-2) and microRNA (miR)-29b. peoniflorin 54-66 microRNA 29b-1 Homo sapiens 199-217 27430753-12 2016 In addition, paeoniflorin was able to induce the expression of miR-29b. peoniflorin 13-25 microRNA 29b-1 Homo sapiens 63-70 27430753-14 2016 In conclusion, the present study demonstrated that paeoniflorin was able to inhibit cell proliferation and promote apoptosis of MM cells by suppressing the expression of MMP-2, via the upregulation of miR-29b. peoniflorin 51-63 microRNA 29b-1 Homo sapiens 201-208 27199349-8 2016 We also noted that miR-29b could confer sensitivity to intrinsic apoptosis triggered by exposure to cisplatin, a drug used widely in lung cancer treatment. Cisplatin 100-109 microRNA 29b-1 Homo sapiens 19-26 26728178-10 2016 Overall, our findings provide novel insights into the molecular mechanism of aldosterone-mediated vascular pathogenesis by identifying miR-29b as a pathophysiologic relevant target of activated MR in VSMCs and by highlighting the importance of miR processing for miR regulation.-Bretschneider, M., Busch, B., Mueller, D., Nolze, A., Schreier, B., Gekle, M., Grossmann, C. Activated mineralocorticoid receptor regulates micro-RNA-29b in vascular smooth muscle cells. Aldosterone 77-88 microRNA 29b-1 Homo sapiens 135-142 27196750-5 2016 Moreover, treatment with the pan-HDAC inhibitor SAHA upregulated miR-29b, overcoming the negative control exerted by HDAC4. Vorinostat 48-52 microRNA 29b-1 Homo sapiens 65-72 27196750-6 2016 Importantly, overexpression or inhibition of miR-29b, respectively, potentiated or antagonized SAHA activity on multiple myeloma cells, as also shown in vivo by a strong synergism between miR-29b synthetic mimics and SAHA in a murine xenograft model of human multiple myeloma. Vorinostat 95-99 microRNA 29b-1 Homo sapiens 45-52 27196750-6 2016 Importantly, overexpression or inhibition of miR-29b, respectively, potentiated or antagonized SAHA activity on multiple myeloma cells, as also shown in vivo by a strong synergism between miR-29b synthetic mimics and SAHA in a murine xenograft model of human multiple myeloma. Vorinostat 95-99 microRNA 29b-1 Homo sapiens 188-195 27196750-6 2016 Importantly, overexpression or inhibition of miR-29b, respectively, potentiated or antagonized SAHA activity on multiple myeloma cells, as also shown in vivo by a strong synergism between miR-29b synthetic mimics and SAHA in a murine xenograft model of human multiple myeloma. Vorinostat 217-221 microRNA 29b-1 Homo sapiens 45-52 25784815-12 2015 Upregulation of miR-29b also enhanced the chemosensitivity of PCa cells to cisplatin. Cisplatin 75-84 microRNA 29b-1 Homo sapiens 16-23 26887789-0 2016 Surface Functionalization of Titanium Alloy with miR-29b Nanocapsules To Enhance Bone Regeneration. Titanium 29-43 microRNA 29b-1 Homo sapiens 49-56 26887789-5 2016 The previous developed nanocapsules were used as the building blocks, and then a bioactive titanium coating was designed to entrap the miR-29b nanocapsules. Titanium 91-99 microRNA 29b-1 Homo sapiens 135-142 26718793-5 2016 The present study investigated the effect of genistein on the proliferation and apoptosis of MM cells through the regulation of nuclear factor-kappaB (NF-kappaB) and microRNA-29b (miR-29b). Genistein 45-54 microRNA 29b-1 Homo sapiens 180-187 26718793-11 2016 Furthermore, it was found that genistein could suppress the protein level of NF-kappaB and promote the expression of miR-29b in U266 cells. Genistein 31-40 microRNA 29b-1 Homo sapiens 117-124 26718793-13 2016 These findings suggest that genistein inhibits the proliferation of human MM cells by upregulating miR-29b resulting in suppression of NF-kappaB. Genistein 28-37 microRNA 29b-1 Homo sapiens 99-106 26818210-5 2016 Recently, we described a new strategy based arginine-affinity chromatography to specifically purify the recombinant pre-miR-29b. Arginine 44-52 microRNA 29b-1 Homo sapiens 120-127 26818210-7 2016 It was verified that Chitosan/pre-miR-29b and Polyethylenimine/pre-miR-29b systems efficiently delivered pre-miR-29b to N2a695 cells, thus reducing the hBACE1 protein expression (around 78% and 86%, respectively) and Abeta42 levels (approximately 44% and 47%, respectively). Polyethyleneimine 46-62 microRNA 29b-1 Homo sapiens 67-74 26126866-7 2015 MiR-29b level negatively associated with NIHSS scores (r=-0.349, P<0.01) and brain infarct volume (r=-0.321, P<0.05). nihss 41-46 microRNA 29b-1 Homo sapiens 0-7 25788572-6 2015 Cellular polyamines were found to regulate miR-29b expression by altering JunD abundance, since the increase in miR-29b expression levels in polyamine-deficient cells was abolished by JunD silencing. Polyamines 9-19 microRNA 29b-1 Homo sapiens 43-50 25788572-6 2015 Cellular polyamines were found to regulate miR-29b expression by altering JunD abundance, since the increase in miR-29b expression levels in polyamine-deficient cells was abolished by JunD silencing. Polyamines 9-19 microRNA 29b-1 Homo sapiens 112-119 25788572-6 2015 Cellular polyamines were found to regulate miR-29b expression by altering JunD abundance, since the increase in miR-29b expression levels in polyamine-deficient cells was abolished by JunD silencing. Polyamines 9-18 microRNA 29b-1 Homo sapiens 43-50 25788572-6 2015 Cellular polyamines were found to regulate miR-29b expression by altering JunD abundance, since the increase in miR-29b expression levels in polyamine-deficient cells was abolished by JunD silencing. Polyamines 9-18 microRNA 29b-1 Homo sapiens 112-119 25356754-4 2015 miR-29b transduction in the liver of mice prevented CCl4 induced-fibrogenesis, concomitant with decreased expression of alpha-SMA, collagen I and TIMP-1. Carbon Tetrachloride 52-56 microRNA 29b-1 Homo sapiens 0-7 26536822-3 2016 In AML cells, PRMT5 interacted with Sp1 in a transcription repressor complex and silenced miR-29b preferentially via dimethylation of histone 4 arginine residue H4R3. Arginine 144-152 microRNA 29b-1 Homo sapiens 90-97 26365178-6 2015 Collectively our findings unravel the means by which MSCT rescues MRL/lpr BMMSC function through reuse of donor exosome-provided Fas to regulate the miR-29b/Dnmt1/Notch epigenetic cascade. ammonium ferrous sulfate 129-132 microRNA 29b-1 Homo sapiens 149-156 26099492-8 2015 Furthermore, oxymatrine decreased the protein levels of MMP-2 and increased the expression levels of miR-29b in OVCAR-3 cells. oxymatrine 13-23 microRNA 29b-1 Homo sapiens 101-108 26099492-10 2015 In addition, anti-miR-29b antibodies were used to verify that the apoptotic effect of oxymatrine was due to upregulating miR-29b and downregulating MMP-2 expression. oxymatrine 86-96 microRNA 29b-1 Homo sapiens 18-25 26099492-10 2015 In addition, anti-miR-29b antibodies were used to verify that the apoptotic effect of oxymatrine was due to upregulating miR-29b and downregulating MMP-2 expression. oxymatrine 86-96 microRNA 29b-1 Homo sapiens 121-128 26099492-11 2015 These results showed that oxymatrine suppresses the proliferation and facilitates apoptosis of human ovarian cancer cells through upregulating miR-29b and downregulating MMP-2 expression. oxymatrine 26-36 microRNA 29b-1 Homo sapiens 143-150 26564501-0 2015 [miR-29b Reduces Cisplatin Resistance of Gastric Cancer Cell by Targeting PI3K/Akt Pathway]. Cisplatin 17-26 microRNA 29b-1 Homo sapiens 1-8 26564501-1 2015 OBJECTIVE: To investigate the regulatory effect of miR-29b on gastric cells" resistance to cisplatin. Cisplatin 91-100 microRNA 29b-1 Homo sapiens 51-58 26564501-2 2015 METHODS: The expression of miR-29b in gastric cancer cell line treated with cisplatin concentration gradient was detected using quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blotting. Cisplatin 76-85 microRNA 29b-1 Homo sapiens 27-34 26564501-3 2015 CCK8 was used to measure the cell viability after cisplatin treatment in condition of miR-29b knock-down and overexpression. Cisplatin 50-59 microRNA 29b-1 Homo sapiens 86-93 26564501-4 2015 RESULTS: The expression of miR-29b was significantly upregualted by cisplatin treatment,while its target gene AKT2 was downregulated. Cisplatin 68-77 microRNA 29b-1 Homo sapiens 27-34 26564501-5 2015 The up-regulation of miR-29b enhanced the sensitivity of gastric cancer cells to cisplatin,while the knock-down of miR-29b enhanced the cisplatin resistance. Cisplatin 81-90 microRNA 29b-1 Homo sapiens 21-28 26564501-5 2015 The up-regulation of miR-29b enhanced the sensitivity of gastric cancer cells to cisplatin,while the knock-down of miR-29b enhanced the cisplatin resistance. Cisplatin 136-145 microRNA 29b-1 Homo sapiens 115-122 26564501-6 2015 Rescue experiments demonstrated that the miR-29b might regulate cisplatin resistance of gastric cancer cell by targeting PI3K/Akt pathway. Cisplatin 64-73 microRNA 29b-1 Homo sapiens 41-48 26175849-3 2015 MATERIALS AND METHODS: In this paper, we explored the expression of miR-29b in a cohort of 67 pairs of formalin-fixed paraffin-embedded specimens with detailed pathological and clinical characteristics, and further analyzed the effects of miR-29b on the malignant phenotype of HER-2-positive breast cancer cells and the relevant mechanisms involved. Formaldehyde 103-111 microRNA 29b-1 Homo sapiens 68-75 26175849-3 2015 MATERIALS AND METHODS: In this paper, we explored the expression of miR-29b in a cohort of 67 pairs of formalin-fixed paraffin-embedded specimens with detailed pathological and clinical characteristics, and further analyzed the effects of miR-29b on the malignant phenotype of HER-2-positive breast cancer cells and the relevant mechanisms involved. Paraffin 118-126 microRNA 29b-1 Homo sapiens 68-75 25234165-0 2015 MiR-29b replacement inhibits proteasomes and disrupts aggresome+autophagosome formation to enhance the antimyeloma benefit of bortezomib. Bortezomib 126-136 microRNA 29b-1 Homo sapiens 0-7 25234165-5 2015 MiR-29b was significantly reduced in bortezomib-resistant cells as well as in cells resistant to second-generation PIs carfilzomib and ixazomib. Bortezomib 37-47 microRNA 29b-1 Homo sapiens 0-7 25234165-5 2015 MiR-29b was significantly reduced in bortezomib-resistant cells as well as in cells resistant to second-generation PIs carfilzomib and ixazomib. carfilzomib 119-130 microRNA 29b-1 Homo sapiens 0-7 25234165-5 2015 MiR-29b was significantly reduced in bortezomib-resistant cells as well as in cells resistant to second-generation PIs carfilzomib and ixazomib. ixazomib 135-143 microRNA 29b-1 Homo sapiens 0-7 25234165-9 2015 Immunofluorescence studies revealed that miR-29b replacements enhanced the bortezomib-induced accumulation of ubiquitinated proteins but did not reveal aggresome or autophagosome formation. Bortezomib 75-85 microRNA 29b-1 Homo sapiens 41-48 25234165-10 2015 Taken together, our study identifies miR-29b replacements as the first-in-class miR-based PIs that also disrupt the autophagy pathway and highlight their potential to synergistically enhance the antimyeloma effect of bortezomib. Bortezomib 217-227 microRNA 29b-1 Homo sapiens 37-44 24554719-6 2014 In the present study, we identified a particular microRNA, miR-29b, as a novel target of ethanol in the developing cerebellar granule neurons. Ethanol 89-96 microRNA 29b-1 Homo sapiens 59-66 25352117-9 2014 Lithium chloride treatment upregulated miR-29b expression, and suppressed the levels of various ECM proteins under both basal and TGF-beta2 stimulatory conditions. Lithium Chloride 0-16 microRNA 29b-1 Homo sapiens 39-46 25032858-7 2014 In addition, miR-29b mediated the inhibition of epithelial-mesenchymal transition (EMT) and the inactivation of mitogen-activated protein kinase and phosphatidylinositol-4,5-bisphosphate 3-kinase/AKT signal transduction pathway. Phosphatidylinositol 4,5-Diphosphate 149-186 microRNA 29b-1 Homo sapiens 13-20 24650661-5 2014 In this study we have demonstrated that expression of HSP47 and LOX was significantly up-regulated in culture-activated primary rat hepatic stellate cells (HSCs), TGF-beta stimulated LX-2 cells and liver tissue of CCl4-treated mice, which was accompanied by a decrease of miR-29b level. Carbon Tetrachloride 214-218 microRNA 29b-1 Homo sapiens 272-279 24992675-11 2014 Upregulation of miR-29b also reduced levels of Mcl-1 and sensitized ES2 cells to low-dose paclitaxel. Paclitaxel 90-100 microRNA 29b-1 Homo sapiens 16-23 25337211-8 2014 Meanwhile miR-29b could induce apoptosis of MG63. mg63 44-48 microRNA 29b-1 Homo sapiens 10-17 24554719-7 2014 We discovered that ethanol exposure suppressed miR-29b and induced neuronal apoptosis. Ethanol 19-26 microRNA 29b-1 Homo sapiens 47-54 24554719-8 2014 Overexpression of miR-29b rendered neurons protection against ethanol-induced apoptosis. Ethanol 62-69 microRNA 29b-1 Homo sapiens 18-25 24554719-9 2014 Furthermore, our data indicated that miR-29b mediated ethanol neurotoxicity through the SP1/RAX/PKR cascade. Ethanol 54-61 microRNA 29b-1 Homo sapiens 37-44 24554719-10 2014 More importantly, the expression of miR-29b is developmentally regulated, which may account for, at least partially, the temporal window of ethanol sensitivity in the developing cerebellum. Ethanol 140-147 microRNA 29b-1 Homo sapiens 36-43 24138392-9 2014 In addition, miR-29b was involved in the hypomethylation of PTEN by curcumin. Curcumin 68-76 microRNA 29b-1 Homo sapiens 13-20 24138392-10 2014 MiR-29b not only was increased by curcumin in activated HSCs, but also was confirmed to target DNMT3b by luciferase activity assays. Curcumin 34-42 microRNA 29b-1 Homo sapiens 0-7 24138392-11 2014 Curcumin-mediated PTEN up-regulation, DNMT3b down-regulation and PTEN hypomethylation were all attenuated by miR-29b inhibitor. Curcumin 0-8 microRNA 29b-1 Homo sapiens 109-116 24138392-12 2014 Collectively, it is demonstrated that curcumin can up-regulate miR-29b expression, resulting in DNMT3b down-regulation in HSCs and epigenetically-regulated PTEN involved in the suppression of activated HSCs. Curcumin 38-46 microRNA 29b-1 Homo sapiens 63-70 23418963-9 2013 Functional overexpression analyses using microRNA mimics revealed that miR-26a/b, as well as miR-29b strongly accelerated osteogenic differentiation of USSC as assessed by Alizarin-Red staining and calcium-release assays. alizarin 172-184 microRNA 29b-1 Homo sapiens 93-100 24147037-0 2013 miR-29b, miR-205 and miR-221 enhance chemosensitivity to gemcitabine in HuH28 human cholangiocarcinoma cells. gemcitabine 57-68 microRNA 29b-1 Homo sapiens 0-7 23178755-0 2013 Increased anti-leukemic activity of decitabine via AR-42-induced upregulation of miR-29b: a novel epigenetic-targeting approach in acute myeloid leukemia. Decitabine 36-46 microRNA 29b-1 Homo sapiens 81-88 23178755-3 2013 Therefore, an increase in miR-29b expression preceding decitabine treatment may provide a therapeutic advantage. Decitabine 55-65 microRNA 29b-1 Homo sapiens 26-33 23178755-6 2013 We hypothesized that priming AML cells with the novel HDAC inhibitor (HDACI) AR-42 would result in increased response to decitabine treatment via upregulation of miR-29b. Decitabine 121-131 microRNA 29b-1 Homo sapiens 162-169 24091729-9 2013 Finally, the proteasome inhibitor bortezomib, which induces the expression of miR-29b, decreased global DNA methylation by a miR-29b-dependent mechanism and induced SOCS-1 promoter demethylation and protein upregulation. Bortezomib 34-44 microRNA 29b-1 Homo sapiens 78-85 24091729-9 2013 Finally, the proteasome inhibitor bortezomib, which induces the expression of miR-29b, decreased global DNA methylation by a miR-29b-dependent mechanism and induced SOCS-1 promoter demethylation and protein upregulation. Bortezomib 34-44 microRNA 29b-1 Homo sapiens 125-132 24091729-10 2013 In conclusion, our data indicate that miR-29b is endowed with epigenetic activity and mediates previously unknown functions of bortezomib in MM cells. Bortezomib 127-137 microRNA 29b-1 Homo sapiens 38-45 23930580-1 2013 We report a simple and sensitive label-free immunosensor for detection of microRNAs (miRNA) based on a conducting polymer/reduced graphene oxide-modified electrode to detect miR-29b-1 and miR-141. graphene oxide 130-144 microRNA 29b-1 Homo sapiens 174-183 23591808-4 2013 We developed a cationic lipoplexes (LPs)-based carrier that efficiently delivered miR-29b both in vitro and in vivo. lps 36-39 microRNA 29b-1 Homo sapiens 82-89 23591808-5 2013 LPs containing miR-29b (LP-miR-29b) efficiently delivered miR-29b to NSCLC A549 cells, reduced the expression of key targets CDK6, DNMT3B, and myeloid cell leukemia sequence 1 (MCL1), as well as cell growth and clonogenicity of A549 cells. lps 0-3 microRNA 29b-1 Homo sapiens 15-22 23591808-5 2013 LPs containing miR-29b (LP-miR-29b) efficiently delivered miR-29b to NSCLC A549 cells, reduced the expression of key targets CDK6, DNMT3B, and myeloid cell leukemia sequence 1 (MCL1), as well as cell growth and clonogenicity of A549 cells. lps 0-3 microRNA 29b-1 Homo sapiens 27-34 23591808-5 2013 LPs containing miR-29b (LP-miR-29b) efficiently delivered miR-29b to NSCLC A549 cells, reduced the expression of key targets CDK6, DNMT3B, and myeloid cell leukemia sequence 1 (MCL1), as well as cell growth and clonogenicity of A549 cells. lps 0-3 microRNA 29b-1 Homo sapiens 27-34 23591808-6 2013 In addition, the IC50 for cisplatin in the miR-29b-treated cells was effectively reduced. Cisplatin 26-35 microRNA 29b-1 Homo sapiens 43-50 23418963-9 2013 Functional overexpression analyses using microRNA mimics revealed that miR-26a/b, as well as miR-29b strongly accelerated osteogenic differentiation of USSC as assessed by Alizarin-Red staining and calcium-release assays. Calcium 198-205 microRNA 29b-1 Homo sapiens 93-100 23100393-6 2012 In vitro transfection of MM cells with synthetic miR-29b mimics significantly impairs cell cycle progression and also potentiates the growth-inhibitory effects induced by the demethylating agent 5-azacitidine. Azacitidine 195-208 microRNA 29b-1 Homo sapiens 49-56 22249264-4 2012 Incubation of lung cancer cells with the Src inhibitor saracatinib led to the upregulation of several miRNAs including miR-29b, which was the most highly upregulated miRNA with predicted binding to the ID1 3"-untranslated region (UTR). saracatinib 55-66 microRNA 29b-1 Homo sapiens 119-126 22249264-9 2012 Both, anti-miR-29b and ID1 overexpression diminished the effects of the Src inhibitors saracatinib and dasatinib on migration and invasion. saracatinib 87-98 microRNA 29b-1 Homo sapiens 11-18 22249264-9 2012 Both, anti-miR-29b and ID1 overexpression diminished the effects of the Src inhibitors saracatinib and dasatinib on migration and invasion. Dasatinib 103-112 microRNA 29b-1 Homo sapiens 11-18 22249264-10 2012 Saracatinib and dasatinib decreased c-Myc transcriptional repression on miR-29b and led to increased ID1 protein levels, whereas forced expression of c-Myc repressed miR-29b and induced ID1. saracatinib 0-11 microRNA 29b-1 Homo sapiens 72-79 22249264-10 2012 Saracatinib and dasatinib decreased c-Myc transcriptional repression on miR-29b and led to increased ID1 protein levels, whereas forced expression of c-Myc repressed miR-29b and induced ID1. Dasatinib 16-25 microRNA 29b-1 Homo sapiens 72-79 22932723-4 2012 In the present study, we demonstrate reduced expression of the tropic factor platelet-derived growth factor (PDGF)-B with a concomitant increase in miR-29b in the basal ganglia region of the brains of morphine-dependent simian immunodeficiency virus (SIV)-infected macaques compared with the SIV-infected controls. Morphine 201-209 microRNA 29b-1 Homo sapiens 148-155 22932723-5 2012 In vitro relevance of these findings was corroborated in cultures of astrocytes exposed to morphine and HIV Tat that led to increased release of miR-29b in exosomes. Morphine 91-99 microRNA 29b-1 Homo sapiens 145-152 22566605-2 2012 Subsequent preclinical studies with bortezomib in AML cells have shown drug-induced miR-29b up-regulation, resulting in loss of transcriptional activation for several genes relevant to myeloid leukemogenesis, including DNA methyltransferases and receptor tyrosine kinases. Bortezomib 36-46 microRNA 29b-1 Homo sapiens 84-91 22566605-8 2012 Additional mechanistic studies showed that FLT3 down-regulation was due to bortezomib-induced miR-29b up-regulation; this led to SP1 down-regulation and destruction of the SP1/NF-kappaB complex that transactivated FLT3. Bortezomib 75-85 microRNA 29b-1 Homo sapiens 94-101