PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32645343-5 2020 Besides, BIBR1532 augmented ATO-induced cytotoxic effects via triggering G1 cell cycle arrest and induction of apoptosis coupled with the down-regulation of NF-kappaB target genes that were involved in cell cycle progression (e.g. CCND1 and CDK6) and prevention of apoptosis such as Bcl-2, Bcl-xl, c-IAP2, and Survivin Respectively. Arsenic Trioxide 28-31 cyclin D1 Homo sapiens 231-236 20862710-8 2010 Inhibiting the activation of Akt and ERK1/2, but not p38 MAPK, decreased the ATO-induced expression of cyclin D1 protein. Arsenic Trioxide 77-80 cyclin D1 Homo sapiens 103-112 19444595-0 2009 Modulation of p53, c-fos, RARE, cyclin A, and cyclin D1 expression in human leukemia (HL-60) cells exposed to arsenic trioxide. Arsenic Trioxide 110-126 cyclin D1 Homo sapiens 46-55 17617380-0 2007 Arsenic trioxide-mediated growth inhibition in gallbladder carcinoma cells via down-regulation of Cyclin D1 transcription mediated by Sp1 transcription factor. Arsenic Trioxide 0-16 cyclin D1 Homo sapiens 98-107 17617380-2 2007 Here, we demonstrated that arsenic trioxide inhibited the proliferation of gallbladder carcinoma in vivo and in vitro as well as the transcription of cell cycle-related protein Cyclin D1. Arsenic Trioxide 27-43 cyclin D1 Homo sapiens 177-186 17617380-3 2007 And, Cyclin D1 overexpression inhibited the negative role of arsenic trioxide in cell cycle progression. Arsenic Trioxide 61-77 cyclin D1 Homo sapiens 5-14 17617380-4 2007 We further explored the mechanisms by which arsenic trioxide affected Cyclin D1 transcription and found that the Sp1 transcription factor was down-regulated by arsenic trioxide, with a corresponding decrease in Cyclin D1 promoter activity. Arsenic Trioxide 44-60 cyclin D1 Homo sapiens 70-79 17617380-4 2007 We further explored the mechanisms by which arsenic trioxide affected Cyclin D1 transcription and found that the Sp1 transcription factor was down-regulated by arsenic trioxide, with a corresponding decrease in Cyclin D1 promoter activity. Arsenic Trioxide 160-176 cyclin D1 Homo sapiens 70-79 17617380-5 2007 Taken together, these results suggested that arsenic trioxide inhibited gallbladder carcinoma cell proliferation via down-regulation of Cyclin D1 transcription in a Sp1-dependent manner, which provided a new mechanism of arsenic trioxide-involved cell proliferation and may have important therapeutic implications in gallbladder carcinoma patients. Arsenic Trioxide 45-61 cyclin D1 Homo sapiens 136-145 17617380-5 2007 Taken together, these results suggested that arsenic trioxide inhibited gallbladder carcinoma cell proliferation via down-regulation of Cyclin D1 transcription in a Sp1-dependent manner, which provided a new mechanism of arsenic trioxide-involved cell proliferation and may have important therapeutic implications in gallbladder carcinoma patients. Arsenic Trioxide 221-237 cyclin D1 Homo sapiens 136-145 20862710-9 2010 This study reports for the first time that p38 MAPK/Akt/ERK1/2 activation is required for the protein stabilization of CDC6 in addition to cyclin D1 in ATO-induced cell proliferation and cell cycle modulation from G1 to S phase. Arsenic Trioxide 152-155 cyclin D1 Homo sapiens 139-148 20435036-3 2010 Using arsenic trioxide-responsive KU7 and non-responsive 253JB-V bladder cancer cells as models, we show that in KU7 cells, < or =5 microM arsenic trioxide decreased Sp1, Sp3 and Sp4 and several Sp-dependent genes and responses including cyclin D1, epidermal growth factor receptor, bcl-2, survivin and vascular endothelial growth factor, whereas at concentrations up to 15 microM, minimal effects were observed in 253JB-V cells. Arsenic Trioxide 142-158 cyclin D1 Homo sapiens 241-250 26359868-10 2015 As2O3 also decreased the protein expressions of cyclin D1, cyclin E, cyclin B1, cyclin-dependent kinase (CDK) 2, and CDK4, but did not affect the protein expressions of p21 and p27. Arsenic Trioxide 0-5 cyclin D1 Homo sapiens 48-57 25258011-0 2014 The influence of arsenic trioxide on the cell cycle, apoptosis and expression of cyclin D1 in the Jurkat cell line. Arsenic Trioxide 17-33 cyclin D1 Homo sapiens 81-90 25258011-3 2014 In this study we aimed to evaluate the expression and localization of cyclin D1 in arsenic trioxide (ATO) treated Jurkat cells (lymphoblastic leukemia cell line) and to correlate these results with the extent of cell death and/or cell cycle alterations. Arsenic Trioxide 83-99 cyclin D1 Homo sapiens 70-79 25258011-3 2014 In this study we aimed to evaluate the expression and localization of cyclin D1 in arsenic trioxide (ATO) treated Jurkat cells (lymphoblastic leukemia cell line) and to correlate these results with the extent of cell death and/or cell cycle alterations. Arsenic Trioxide 101-104 cyclin D1 Homo sapiens 70-79 25258011-9 2014 On the other hand, we found a nuclear-cytoplasmic shift of this protein as a major treatment-related response, which was in good accord with an increased rate of cell death and suggested that cyclin D1 cytoplasmic degradation is an important determinant of the therapeutic efficiency of ATO in the Jurkat cell line. Arsenic Trioxide 287-290 cyclin D1 Homo sapiens 192-201 23255470-3 2014 In the NuLi-1 immortalized human lung epithelial cell line with p53 and pRb deficiency, exposure to low doses of arsenic trioxide for 72 h promoted cell proliferation and upregulated the gene transcription levels of FOXM1, CDC6, CDC25A, and cyclin D1, which are both critical cell cycle regulatory genes and proto-oncogenes. Arsenic Trioxide 113-129 cyclin D1 Homo sapiens 241-250 29159499-6 2018 Analysis of promoter methylation status of 22 cell cycle related genes in NB4 revealed that CCND1, CCNE1, CCNF, CDKN1A, GADD45alpha, and RBL1 genes were methylated 60.7, 84.6, 58.6, 8.7, 33.4, and 73.7%, respectively, that after treatment with 2 muM ATO for 48 h, turn into 0.6, 13.8, 0.1, 6.6, 10.7, and 54.5% methylated. Arsenic Trioxide 250-253 cyclin D1 Homo sapiens 92-97 29159499-8 2018 ATO induced the expression of CCND1, CCNE1, and GADD45alpha genes, suppressed the expression of CCNF and CDKN1A genes, which were consistent with decreased number of cells in G1 and S phases and increased number of cells in G2/M phase. Arsenic Trioxide 0-3 cyclin D1 Homo sapiens 30-35 29442453-10 2017 CONCLUSIONS: The overall results indicate that CCND1, FOXO1, and JUN may contribute to the induction of resistance to ATO, and that the C-Jun N-terminal kinase (JNK) signaling pathway may have greater significance than the phosphoinositide 3-kinase (PI3K)/Akt pathway in mediating the cytotoxic effects of ATO and the development of resistance to ATO in the HL-60 cell line. Arsenic Trioxide 118-121 cyclin D1 Homo sapiens 47-52 29059232-6 2017 We found that ATO treatment of HeLa cells resulted in significant decreases in the expression of beta-catenin mRNA and protein and the downstream target factors c-Myc, cyclin B1, and cyclin D1 in the Wnt signaling pathway. Arsenic Trioxide 14-17 cyclin D1 Homo sapiens 183-192 28024484-4 2016 The expression of CyclinD1 and p27kip1 in K562 cells treated with As2O3 was analyzed by reverse transcription-polymerase chain reaction(RT-PCR), immunohistochemistry and Western blot. Arsenic Trioxide 66-71 cyclin D1 Homo sapiens 18-26 28024484-7 2016 As2O3 could markedly inhibit the expression of CyclinD1 in K562 cells(P<0.05), but the expression of P27kip1 was not significantly changed after As2O3 treatment. Arsenic Trioxide 0-5 cyclin D1 Homo sapiens 47-55 28024484-8 2016 CONCLUSIONS: As2O3 can induce K562 cell apoptosis and inhibit K562 cell proliferation by regulating the expression of CyclinD1. Arsenic Trioxide 13-18 cyclin D1 Homo sapiens 118-126 25945059-8 2015 Arsenic trioxide treatment also reduced Gli1 downstream target gene expression, such as Bcl2 and CCND1. Arsenic Trioxide 0-16 cyclin D1 Homo sapiens 97-102 25416439-6 2015 Both sorafenib and ATO downregulated the expression of cyclin D1, resulting in HCC cells arrested at G0/G1 phase. Arsenic Trioxide 19-22 cyclin D1 Homo sapiens 55-64 23949314-0 2014 Arsenic trioxide suppressed mantle cell lymphoma by downregulation of cyclin D1. Arsenic Trioxide 0-16 cyclin D1 Homo sapiens 70-79 23949314-4 2014 In MCL lines Jeko-1 and Granta-519, As2O3 induced dose-dependent and time-dependent increases in apoptosis accompanied by cyclin D1 suppression. Arsenic Trioxide 36-41 cyclin D1 Homo sapiens 122-131 23949314-7 2014 Instead, As2O3 activated glycogen synthase kinase-3beta (by tyrosine-216 phosphorylation) and IkappaB kinase alpha/beta (by serine-176/180 phosphorylation), both of which phosphorylated cyclin D1 at threonine-286, leading to its poly-ubiquitination and degradation in the proteasome. Arsenic Trioxide 9-14 cyclin D1 Homo sapiens 186-195 23911876-10 2013 On the other hand, changes in expression of cyclin D1 (CCND1), insulin receptor substrate 1 (IRS1) and protein kinase C isoforms (PRKCZ,PRKCB and PRKCA) may be responsible for the induction of resistance to ATO. Arsenic Trioxide 207-210 cyclin D1 Homo sapiens 44-53