PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35315497-0 2022 Long non-coding RNA MALAT1 is involved in retinal pigment epithelial cell damage caused by high glucose treatment. Glucose 96-103 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 20-26 34478876-5 2021 Further investigation showed that MALAT1 knockdown inhibited glucose uptake and lipogenesis by reducing the expression levels of these lipid metabolism related genes, which contributes to the oncogenic role of MALAT1 in tumor cell proliferation and invasion. Glucose 61-68 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 34-40 34478876-5 2021 Further investigation showed that MALAT1 knockdown inhibited glucose uptake and lipogenesis by reducing the expression levels of these lipid metabolism related genes, which contributes to the oncogenic role of MALAT1 in tumor cell proliferation and invasion. Glucose 61-68 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 210-216 35315497-1 2022 The present study aimed to explore the role of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) in high glucose (HG)-induced ARPE-19 cell damage. Glucose 146-153 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 130-136 32502356-0 2020 Inhibition of long noncoding RNA MALAT1 suppresses high glucose-induced apoptosis and inflammation in human umbilical vein endothelial cells by suppressing the NF-kappaB signaling pathway. Glucose 56-63 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 33-39 33887222-0 2021 Knockdown of Malat1 alleviates high-glucose-induced angiogenesis through regulating miR-205-5p/VEGF-A axis. Glucose 36-43 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 13-19 33887222-3 2021 In this research, Malat1, miR-205-5p, and VEGF-A levels in high glucose (HG) treat-human retinal microvascular endothelial cells (hRMECs) was detected with qRT-PCR. Glucose 64-71 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 18-24 33051272-6 2021 Glucose increased LncRNA MALAT1 levels by increasing Sp1 transcription factor binding at its promoter. Glucose 0-7 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 25-31 33051272-7 2021 Downregulation of LncRNA MALAT1 by its siRNA prevented glucose-induced increase in Keap1, and facilitated Nrf2 nuclear translocation and antioxidant gene transcription. Glucose 55-62 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 25-31 32502356-1 2020 The study aimed to investigate the expression of long noncoding RNA (lncRNA) MALAT1 in high glucose (HG)-induced human vascular endothelial cells (HUVECs) and the role of MALAT1 in the apoptosis of HG-induced HUVECs. Glucose 92-99 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 77-83 32391974-0 2020 LncRNA MALAT1 promoted high glucose-induced pyroptosis of renal tubular epithelial cell by sponging miR-30c targeting for NLRP3. Glucose 28-35 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 7-13 33274006-4 2020 This study is aimed at investigating the function and mechanism of MALAT1 in the regulation of EMT in human LECs under high glucose conditions. Glucose 124-131 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 67-73 32691071-0 2020 Retraction: LncRNA MALAT1up-regulates VEGF-A and ANGPT2 to promote angiogenesis in brain microvascular endothelial cells against oxygen-glucose deprivation via targeting miR-145. Glucose 136-143 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 19-25 31388927-0 2019 lncRNA MALAT1 mediated high glucose-induced HK-2 cell epithelial-to-mesenchymal transition and injury. Glucose 28-35 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 7-13 32579210-0 2020 Expression of Concern: LncRNA MALAT1 up-regulates VEGF-A and ANGPT2 to promote angiogenesis in brain microvascular endothelial cells against oxygen-glucose deprivation via targetting miR-145. Glucose 148-155 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 30-36 31823095-0 2019 LncRNA MALAT1 Promotes Oxygen-Glucose Deprivation and Reoxygenation Induced Cardiomyocytes Injury Through Sponging miR-20b to Enhance beclin1-Mediated Autophagy. Glucose 30-37 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 7-13 32509100-0 2020 Long noncoding RNA MALAT1 promotes high glucose-induced inflammation and apoptosis of vascular endothelial cells by regulating miR-361-3p/SOCS3 axis. Glucose 40-47 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 19-25 32323759-0 2020 Long non-coding RNA MALAT1 promotes high glucose-induced rat cartilage endplate cell apoptosis via the p38/MAPK signalling pathway. Glucose 41-48 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 20-26 32323759-4 2020 The aim of the present study was to evaluate the roles of MALAT1 in the apoptosis of cartilage endplate (CEP) cells induced by high glucose and to explore the mechanisms underlying this effect. Glucose 132-139 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 58-64 32323759-9 2020 The results revealed that high glucose concentration promoted apoptosis and enhanced expression of MALAT1 in CEP cells. Glucose 31-38 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 99-105 31986419-0 2020 Knockdown of MALAT1 attenuates high-glucose-induced angiogenesis and inflammation via endoplasmic reticulum stress in human retinal vascular endothelial cells. Glucose 36-43 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 13-19 31856403-4 2020 Among them, MALAT1 attracted more attention as it was profoundly expressed in endothelial cells or cardiomyocytes in response to the risk factors of CVD, such as hypoxia, high glucose, cytokine, and oxidative stress. Glucose 176-183 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 12-18 30762931-3 2019 Hence, this study aimed to explore the role of MALAT1 in high glucose (HG)-induced HRGECs injury and the underlying epigenetic mechanism. Glucose 62-69 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 47-53 31646587-0 2019 LncRNA MALAT1 affects high glucose-induced endothelial cell proliferation, apoptosis, migration and angiogenesis by regulating the PI3K/Akt signaling pathway. Glucose 27-34 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 7-13 31646587-1 2019 OBJECTIVE: To investigate the effects of long non-coding ribonucleic acid (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on the high glucose-induced proliferation, apoptosis, migration and angiogenesis of endothelial cells and its potential mechanism. Glucose 159-166 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 83-137 31646587-1 2019 OBJECTIVE: To investigate the effects of long non-coding ribonucleic acid (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on the high glucose-induced proliferation, apoptosis, migration and angiogenesis of endothelial cells and its potential mechanism. Glucose 159-166 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 139-145 31646587-9 2019 According to wound-healing assay, the knockdown of lncRNA MALAT1 could prominently reverse the declined HUVECs migratory ability induced by high glucose (p<0.05). Glucose 145-152 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 58-64 31646587-12 2019 It was revealed in Western blotting that the knockdown of lncRNA MALAT1 could reverse the inhibition of high glucose on the PI3K/Akt signaling pathway in HUVECs (p<0.05). Glucose 109-116 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 65-71 30762931-0 2019 Long noncoding RNA MALAT1 mediates high glucose-induced glomerular endothelial cell injury by epigenetically inhibiting klotho via methyltransferase G9a. Glucose 40-47 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 19-25 25787249-1 2015 To examine whether the long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is altered in the endothelial cells in response to glucose and the significance of such alteration. Glucose 167-174 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 108-114 30815547-2 2018 Results: Findings from our in vitro experiments demonstrated that MALAT1 was predominantly localized to nuclear speckles in endothelial cells and MALAT1 expression was significantly increased following incubation with high glucose in association with increased expression of inflammatory cytokines. Glucose 223-230 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 66-72 30815547-2 2018 Results: Findings from our in vitro experiments demonstrated that MALAT1 was predominantly localized to nuclear speckles in endothelial cells and MALAT1 expression was significantly increased following incubation with high glucose in association with increased expression of inflammatory cytokines. Glucose 223-230 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 146-152 30132842-2 2018 As an important stress response molecule, MALAT1 can be expressed differently under stress conditions, such as hypoxia, high glucose, hydrogen peroxide, ultraviolet irradiation, infection, and chemical stimulation. Glucose 125-132 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 42-48 30914432-9 2019 Knockdown of TCF7L2 in MALAT1-overexpressing cells and HCC cell lines affected their metabolism and abolished their tumorigenic potential, suggesting that the effects of MALAT1 on glucose metabolism are essential for its oncogenic activity. Glucose 180-187 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 170-176 30591217-0 2019 Long noncoding RNA MALAT1 promotes high glucose-induced human endothelial cells pyroptosis by affecting NLRP3 expression through competitively binding miR-22. Glucose 40-47 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 19-25 30591217-6 2019 Then, we investigated lncRNA MALAT1 expression and found that it was upregulated in high glucose-treated EA.hy926 cells. Glucose 89-96 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 29-35 30591217-7 2019 Furthermore, lncRNA MALAT1 knockdown significantly inhibited high glucose-induced pyroptosis in EA.hy926 cells, which may critically influence atherosclerosis. Glucose 66-73 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 20-26 30591217-10 2019 Ultimately, miR-22 overexpression abrogated the effect of MALAT1 on high glucose-induced EA.hy926 cells pyroptosis. Glucose 73-80 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 58-64 30591217-11 2019 Together, our results suggest that lncRNA MALAT1 promotes high glucose-induced pyroptosis of endothelial cells partly by affecting NLRP3 expression through competitively binding miR-22. Glucose 63-70 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 42-48 29936249-8 2018 RESULTS: MALAT1 not only was aberrantly expressed in DC anterior lens capsule tissues and high glucose (HG)-treated HLECs, but also were up-regulated by HG to promote the apoptosis and oxidative stress of HLECs. Glucose 95-102 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 9-15 29947532-8 2018 While, knocking down the pathogenetic lncRNAs ANRIL, MALAT1, and ZFAS1 subsequently prevented the glucose-induced upregulation of ET-1 transcripts. Glucose 98-105 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 53-59 29317209-0 2018 LncRNA MALAT1 is up-regulated in diabetic gastroparesis and involved in high-glucose-induced cellular processes in human gastric smooth muscle cells. Glucose 77-84 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 7-13 29317209-8 2018 Ultimately, we found that the regulation of MALAT1 expression modulated the function of high-glucose stimulation in human gastric SMCs. Glucose 93-100 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 44-50 27964927-5 2017 Our data demonstrated that MALAT1 expression was substantially increased but miR-23c was decreased in streptozotocin-induced diabetic rats and in high-glucose-treated HK-2 cells. Glucose 151-158 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 27-33 25787249-3 2015 We found an increase in MALAT1 expression peaking after 12 hrs of incubation in high glucose. Glucose 85-92 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 24-30 25787249-7 2015 Results of this study indicate that LncRNA MALAT1 regulates glucose-induced up-regulation of inflammatory mediators IL-6 and TNF-alpha through activation of SAA3. Glucose 60-67 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 43-49 34943778-6 2021 Using human retinal endothelial cells, the effect of high glucose on LncMALAT1 and LncNEAT1 mitochondrial localization was examined by RNA fluorescence in situ hybridization. Glucose 58-65 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 69-78 34943778-8 2021 High glucose increased LncMALAT1 and LncNEAT1 mitochondrial expression, and MALAT1-siRNA or NEAT1-siRNA ameliorated glucose-induced damage to mitochondrial membrane potential and mtDNA, and prevented decrease in mtDNA nucleoids. Glucose 5-12 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 23-32 34943778-8 2021 High glucose increased LncMALAT1 and LncNEAT1 mitochondrial expression, and MALAT1-siRNA or NEAT1-siRNA ameliorated glucose-induced damage to mitochondrial membrane potential and mtDNA, and prevented decrease in mtDNA nucleoids. Glucose 116-123 metastasis associated lung adenocarcinoma transcript 1 Homo sapiens 76-82