PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33386469-9 2021 Western blotting assays showed that the expression levels of EZH2 and cyclin-D1 proteins in arsenite-transformed cells increased. arsenite 92-100 cyclin D1 Homo sapiens 70-79 30066004-5 2018 Chronic arsenite exposure also led to an upregulation of proliferation factors such as cyclin D1, COX2, PCNA, VEGF, and HIF-1alpha. arsenite 8-16 cyclin D1 Homo sapiens 87-96 29528074-0 2018 Arsenite increases Cyclin D1 expression through coordinated regulation of the Ca2+/NFAT2 and NF-kappaB pathways via ERK/MAPK in a human uroepithelial cell line. arsenite 0-8 cyclin D1 Homo sapiens 19-28 29528074-5 2018 Cyclin D1 is known as a proto-oncogene and the level of this protein was increased in SV-HUC-1 cells treated with arsenite for 24 h and long-term. arsenite 114-122 cyclin D1 Homo sapiens 0-9 29528074-8 2018 The results suggest that regulation of Cyclin D1 protein expression by arsenite in SV-HUC-1 cells is dependent on ERK/NFAT2 and ERK/NF-kappaB, but is not dependent on JNK or p38. arsenite 71-79 cyclin D1 Homo sapiens 39-48 28444938-4 2017 mRNA and protein expressions of proliferation factors, such as cyclin D1, COX-2, and proliferating cell nuclear antigen (PCNA), increased in chronically exposed arsenite SV-HUC-1 cells with exposure time. arsenite 161-169 cyclin D1 Homo sapiens 63-72 28444938-6 2017 Knockdown of STAT3 reduced expressions of cyclin D1, COX-2, PCNA, and BCL2 induced by arsenite. arsenite 86-94 cyclin D1 Homo sapiens 42-51 28444938-7 2017 In conclusion, arsenic induced proliferation in human uroepithelial cells after short and long term exposure to arsenite and JAK2/STAT3 signaling pathway might be pivotal in arsenite-induced proliferation by regulating cyclin D1, COX-2, PCNA, and BCL2. arsenite 174-182 cyclin D1 Homo sapiens 219-228 30090515-5 2017 The results showed that low concentration arsenite increased the expressions of proliferative factors BCL2, cyclin D1, COX-2, MMP1 and PCNA in SV-HUC-1 cells, and ATF2 siRNA partly decreased the expressions of BCL2, cyclin D1, and COX-2. arsenite 42-50 cyclin D1 Homo sapiens 108-117 30090515-5 2017 The results showed that low concentration arsenite increased the expressions of proliferative factors BCL2, cyclin D1, COX-2, MMP1 and PCNA in SV-HUC-1 cells, and ATF2 siRNA partly decreased the expressions of BCL2, cyclin D1, and COX-2. arsenite 42-50 cyclin D1 Homo sapiens 216-225 28062277-6 2017 In these cells, arsenite induced increases of EZH2 and cyclin D1 and accelerated the cell cycle. arsenite 16-24 cyclin D1 Homo sapiens 55-64 28062277-8 2017 Further, in HaCaT cells exposed to arsenite, EZH2 regulated the cell cycle by binding to the promoter of CCND1, which codes for cyclin D1. arsenite 35-43 cyclin D1 Homo sapiens 105-110 28062277-8 2017 Further, in HaCaT cells exposed to arsenite, EZH2 regulated the cell cycle by binding to the promoter of CCND1, which codes for cyclin D1. arsenite 35-43 cyclin D1 Homo sapiens 128-137 28062277-11 2017 These results suggest that, in HaCaT cells, arsenite increases circ100284 levels, which act as a sponge for miR-217 and up-regulate the miR-217 target, EZH2, which, in turn, up-regulates cyclin D1and CDK4, and thus accelerates the cell cycle and leads to malignant transformation. arsenite 44-52 cyclin D1 Homo sapiens 187-196 27347121-6 2016 In AsPC-1 cells, the levels of cyclin D1 and phosphorylated retinoblastoma protein decreased following treatment with arsenite, but this was not observed in BxPC-3 cells. arsenite 118-126 cyclin D1 Homo sapiens 31-40 21726611-0 2011 Up-regulation of cyclin D1 by JNK1/c-Jun is involved in tumorigenesis of human embryo lung fibroblast cells induced by a low concentration of arsenite. arsenite 142-150 cyclin D1 Homo sapiens 17-26 21726611-6 2011 Moreover, arsenite activates the JNK1/c-Jun signal pathway, but not JNK2, which up-regulates the expression of cyclin D1/CDK4 and phosphorylates the retinoblastoma (Rb) protein. arsenite 10-18 cyclin D1 Homo sapiens 111-120 21726611-7 2011 Blocking of the JNK1/c-Jun signal pathway suppresses the increases of cyclin D1 expression and Rb phosphorylation, which attenuates cell proliferation, reduces the transition from the G1 to the S phase, and thereby inhibits the neoplastic transformation of HELF cells induced by a low concentration of arsenite. arsenite 302-310 cyclin D1 Homo sapiens 70-79 21726611-8 2011 Thus, activation of the JNK1/c-Jun pathway up-regulates the expression of cyclin D1, which is involved in the tumorigenesis caused by a low concentration of arsenite. arsenite 157-165 cyclin D1 Homo sapiens 74-83 21040761-10 2011 In addition, the Cyclin-D1 increased expression but decreased p16 expression in arsenite-treated SV-HUC-1 cells. arsenite 80-88 cyclin D1 Homo sapiens 17-26 21040761-11 2011 However, when cells were pretreated with inhibitors (5-aza-CdR or U0126), the effects of arsenite on Cyclin-D1 and p16 expression were suppressed. arsenite 89-97 cyclin D1 Homo sapiens 101-110 22102309-0 2011 Induction of cyclin D1 by arsenite and UVB-irradiation in human keratinocytes. arsenite 26-34 cyclin D1 Homo sapiens 13-22 22102309-5 2011 Here, we employed this system to demonstrate concordant cyclin D1-related induction profiles of ultraviolet B radiation and arsenite using cDNA microarray analysis. arsenite 124-132 cyclin D1 Homo sapiens 56-65 20862710-0 2010 Activation of the p38 MAPK/Akt/ERK1/2 signal pathways is required for the protein stabilization of CDC6 and cyclin D1 in low-dose arsenite-induced cell proliferation. arsenite 130-138 cyclin D1 Homo sapiens 108-117 20420878-0 2010 p52-Bcl3 complex promotes cyclin D1 expression in BEAS-2B cells in response to low concentration arsenite. arsenite 97-105 cyclin D1 Homo sapiens 26-35 20420878-3 2010 It is also known that arsenite exposure enhances cyclin D1 expression, which involves NF-kappaB activation. arsenite 22-30 cyclin D1 Homo sapiens 49-58 20420878-7 2010 To profile the canonical and non-canonical NF-kappaB pathways involved in cell growth and cyclin D1 expression induced by low concentration arsenite, the NF-kappaB-specific inhibitor-phenethyl caffeate (CAPE) and NF-kappaB2 mRNA target sequences were used, and cyclin D1 expression in BEAS-2B cells was assessed. arsenite 140-148 cyclin D1 Homo sapiens 90-99 20420878-7 2010 To profile the canonical and non-canonical NF-kappaB pathways involved in cell growth and cyclin D1 expression induced by low concentration arsenite, the NF-kappaB-specific inhibitor-phenethyl caffeate (CAPE) and NF-kappaB2 mRNA target sequences were used, and cyclin D1 expression in BEAS-2B cells was assessed. arsenite 140-148 cyclin D1 Homo sapiens 261-270 20420878-8 2010 Our results demonstrated that exposure to low concentration arsenite enhanced BEAS-2B cells growth and cyclin D1 mRNA and protein expression. arsenite 60-68 cyclin D1 Homo sapiens 103-112 20420878-9 2010 Activation and nuclear localization of p52 and Bcl3 in response to low concentration arsenite indicated that the non-canonical NF-kappaB pathway was involved in arsenite-induced cyclin D1 expression. arsenite 85-93 cyclin D1 Homo sapiens 178-187 20420878-9 2010 Activation and nuclear localization of p52 and Bcl3 in response to low concentration arsenite indicated that the non-canonical NF-kappaB pathway was involved in arsenite-induced cyclin D1 expression. arsenite 161-169 cyclin D1 Homo sapiens 178-187 20420878-11 2010 The up-regulation of cyclin D1 mediated by the p52-Bcl3 complex in response to low concentration arsenite might be important in assessing the health risk of low concentration arsenite and understanding the mechanisms of the harmful effects of arsenite. arsenite 97-105 cyclin D1 Homo sapiens 21-30 20420878-11 2010 The up-regulation of cyclin D1 mediated by the p52-Bcl3 complex in response to low concentration arsenite might be important in assessing the health risk of low concentration arsenite and understanding the mechanisms of the harmful effects of arsenite. arsenite 175-183 cyclin D1 Homo sapiens 21-30 20420878-11 2010 The up-regulation of cyclin D1 mediated by the p52-Bcl3 complex in response to low concentration arsenite might be important in assessing the health risk of low concentration arsenite and understanding the mechanisms of the harmful effects of arsenite. arsenite 175-183 cyclin D1 Homo sapiens 21-30 19519318-0 2009 PI3K/Akt/JNK/c-Jun signaling pathway is a mediator for arsenite-induced cyclin D1 expression and cell growth in human bronchial epithelial cells. arsenite 55-63 cyclin D1 Homo sapiens 72-81 19519318-3 2009 In this study, we demonstrated that arsenite upregulates cyclin D1 expression/activity to promote the growth of human bronchial epithelial Beas-2B cells. arsenite 36-44 cyclin D1 Homo sapiens 57-66 19519318-5 2009 The inhibition of JNKs or c-Jun by chemical or genetic inhibitors blocks the cyclin D1 induction mediated by arsenite. arsenite 109-117 cyclin D1 Homo sapiens 77-86 18197291-0 2008 PI-3K/Akt pathway-dependent cyclin D1 expression is responsible for arsenite-induced human keratinocyte transformation. arsenite 68-76 cyclin D1 Homo sapiens 28-37 18197291-3 2008 OBJECTIVES: In this study, we investigated the potential role of PI-3K/Akt/cyclin D1in the transformation of human keratinocytic cells upon arsenite exposure. arsenite 140-148 cyclin D1 Homo sapiens 75-84 18197291-9 2008 Furthermore, our data also indicated that cyclin D1 is an important downstream molecule involved in PI-3K/Akt-mediated cell transformation upon arsenite exposure based on the facts that inhibition of cyclin D1 expression by dominant negative mutants of PI-3K, and Akt, or the knockdown of the cyclin D1 expression by its specific siRNA in the HaCat cells resulted in impairing of anchorage-independent growth of HaCat cells induced by arsenite. arsenite 144-152 cyclin D1 Homo sapiens 42-51 18197291-9 2008 Furthermore, our data also indicated that cyclin D1 is an important downstream molecule involved in PI-3K/Akt-mediated cell transformation upon arsenite exposure based on the facts that inhibition of cyclin D1 expression by dominant negative mutants of PI-3K, and Akt, or the knockdown of the cyclin D1 expression by its specific siRNA in the HaCat cells resulted in impairing of anchorage-independent growth of HaCat cells induced by arsenite. arsenite 144-152 cyclin D1 Homo sapiens 200-209 18197291-9 2008 Furthermore, our data also indicated that cyclin D1 is an important downstream molecule involved in PI-3K/Akt-mediated cell transformation upon arsenite exposure based on the facts that inhibition of cyclin D1 expression by dominant negative mutants of PI-3K, and Akt, or the knockdown of the cyclin D1 expression by its specific siRNA in the HaCat cells resulted in impairing of anchorage-independent growth of HaCat cells induced by arsenite. arsenite 144-152 cyclin D1 Homo sapiens 200-209 18197291-9 2008 Furthermore, our data also indicated that cyclin D1 is an important downstream molecule involved in PI-3K/Akt-mediated cell transformation upon arsenite exposure based on the facts that inhibition of cyclin D1 expression by dominant negative mutants of PI-3K, and Akt, or the knockdown of the cyclin D1 expression by its specific siRNA in the HaCat cells resulted in impairing of anchorage-independent growth of HaCat cells induced by arsenite. arsenite 435-443 cyclin D1 Homo sapiens 42-51 18197291-10 2008 CONCLUSION: Our results demonstrate that PI-3K/Akt-mediated cyclin D1 expression is at least one key event implicated in the arsenite human skin carcinogenic effect. arsenite 125-133 cyclin D1 Homo sapiens 60-69 17370311-0 2007 PI-3K/Akt signal pathway plays a crucial role in arsenite-induced cell proliferation of human keratinocytes through induction of cyclin D1. arsenite 49-57 cyclin D1 Homo sapiens 129-138 17370311-4 2007 Taken together, we provide the direct evidence that PI-3K/Akt pathway plays a role in the regulation of cell proliferation through the induction of cyclin D1 in human keratinocytes upon arsenite treatment. arsenite 186-194 cyclin D1 Homo sapiens 148-157 17370311-5 2007 Given the importance of aberrant cell proliferation in cell transformation, we propose that the activation of PI-3K/Akt pathway and cyclin D1 induction may be the important mediators of human skin carcinogenic effect of arsenite. arsenite 220-228 cyclin D1 Homo sapiens 132-141 17005224-0 2006 Induction of cyclin D1 by submicromolar concentrations of arsenite in human epidermal keratinocytes. arsenite 58-66 cyclin D1 Homo sapiens 13-22 17005224-6 2006 Real-time PCR analysis of cyclin D1 transcription showed that there was an induction of more than three-fold in cells exposed to 400 nM arsenite for 3 days. arsenite 136-144 cyclin D1 Homo sapiens 26-35 16387740-3 2006 Cyclin D1, a nuclear protein playing a pivotal role in cell proliferation and cell cycle transition from G1 to S phases, has been reported to be induced in human fibroblast by arsenite via uncertain molecular mechanisms. arsenite 176-184 cyclin D1 Homo sapiens 0-9 16230390-0 2005 Cyclin D1 induction through IkappaB kinase beta/nuclear factor-kappaB pathway is responsible for arsenite-induced increased cell cycle G1-S phase transition in human keratinocytes. arsenite 97-105 cyclin D1 Homo sapiens 0-9 16230390-4 2005 Further studies found that arsenite exposure was able to induce cyclin D1 expression. arsenite 27-35 cyclin D1 Homo sapiens 64-73 16230390-5 2005 The induction of cyclin D1 by arsenite required nuclear factor-kappaB (NF-kappaB) activation, because the inhibition of IkappaB phosphorylation by overexpression of the dominant-negative mutant, IKKbeta-KM, impaired arsenite-induced cyclin D1 expression and G1-S transition. arsenite 30-38 cyclin D1 Homo sapiens 17-26 16230390-5 2005 The induction of cyclin D1 by arsenite required nuclear factor-kappaB (NF-kappaB) activation, because the inhibition of IkappaB phosphorylation by overexpression of the dominant-negative mutant, IKKbeta-KM, impaired arsenite-induced cyclin D1 expression and G1-S transition. arsenite 30-38 cyclin D1 Homo sapiens 233-242 16230390-5 2005 The induction of cyclin D1 by arsenite required nuclear factor-kappaB (NF-kappaB) activation, because the inhibition of IkappaB phosphorylation by overexpression of the dominant-negative mutant, IKKbeta-KM, impaired arsenite-induced cyclin D1 expression and G1-S transition. arsenite 216-224 cyclin D1 Homo sapiens 17-26 16230390-7 2005 In addition, knockdown of cyclin D1 expression using cyclin D1-specific small interference RNA significantly blocked arsenite-induced cell cycle progression in HaCat cells. arsenite 117-125 cyclin D1 Homo sapiens 26-35 16230390-7 2005 In addition, knockdown of cyclin D1 expression using cyclin D1-specific small interference RNA significantly blocked arsenite-induced cell cycle progression in HaCat cells. arsenite 117-125 cyclin D1 Homo sapiens 53-62 16230390-8 2005 Taken together, our results show that arsenite-induced cell cycle from G(1) to S phase transition is through IKKbeta/NF-kappaB/cyclin D1-dependent pathway. arsenite 38-46 cyclin D1 Homo sapiens 127-136 11406180-7 2001 In addition, long-term, low dose (but not short-term, high dose) exposure to arsenite resulted in increased expression of cyclin D1. arsenite 77-85 cyclin D1 Homo sapiens 122-131 10952989-2 2000 Exposition of Granta 519 cells to osmotic shock, oxidative stress, and arsenite induced the post-transcriptional down-regulation of cyclin D1. arsenite 71-79 cyclin D1 Homo sapiens 132-141