PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32660355-5 2021 Treatment with 5- azacytidine, markedly decreased expression of UGT2B15 and UGT2B17 over 85% as well as significantly decreased expression of DNMT3B, but not the expression of DNMT3A. Azacitidine 15-29 DNA methyltransferase 3 beta Homo sapiens 142-148 21359954-6 2012 5-aza treatment of DNMT3b KD cells reduced the IC(50) for DOX to 0.036 muM (59%), for PAX to 0.313 nM (37%) and for 5-FU to 0.067 (92%). Azacitidine 0-5 DNA methyltransferase 3 beta Homo sapiens 19-25 30139210-5 2018 Also treatment with CPUK02 decreased the expression of both DNMT3A and DNMT3B genes like 5-AZA.The expression of DNMT genes were diminished by half compared with control cells. Azacitidine 89-94 DNA methyltransferase 3 beta Homo sapiens 71-77 28090275-12 2017 CONCLUSION: In this study, positive correlation was found between mRNA expression of DNMT3b and gene promoter hypermethylation after treatment with CPUK02 and 5-AZA. Azacitidine 159-164 DNA methyltransferase 3 beta Homo sapiens 85-91 23300844-2 2012 In prior work we found that EC cells are hypersensitive to low nanomolar doses of 5-aza deoxycytidine (5-aza) and that this hypersensitivity partially depended on unusually high levels of the DNA methyltransferase, DNMT3B. Azacitidine 82-87 DNA methyltransferase 3 beta Homo sapiens 215-221 23300844-6 2012 Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. Azacitidine 52-57 DNA methyltransferase 3 beta Homo sapiens 109-115 28462005-12 2017 As part of the feedback response, 5-aza increased the expression of the DNA methyltransferases 1 (DNMT1) (P=0.005) and DNMT3B (P=0.002), which are enzymes responsible for gene methylation. Azacitidine 34-39 DNA methyltransferase 3 beta Homo sapiens 119-125 28090275-10 2017 The average expression levels of DNMT3b in HCT116 treated with CPUK02 and 5-AZA relative to the GAPDH expression level in control were 0.16 and 0.5%, respectively. Azacitidine 74-79 DNA methyltransferase 3 beta Homo sapiens 33-39 25746661-7 2015 Specifically, the treatment of two BL cell lines with the DNMT inhibitor 5-aza-dC decreased DNMT1 and DNMT3B protein levels and inhibited cell growth. Azacitidine 73-78 DNA methyltransferase 3 beta Homo sapiens 102-108 25621113-4 2015 Epigenetic therapy by targeting DNA methyltransferases (DNMT) 1, DNMT3A and DNMT3B via 5-Azacytidine (Aza) and 5-Aza-2"-deoxycytidine (Aza-dC) has proved to be successful toward treatment of hematologic neoplasms especially for patients with myelodysplastic syndrome. Azacitidine 87-100 DNA methyltransferase 3 beta Homo sapiens 76-82 25621113-4 2015 Epigenetic therapy by targeting DNA methyltransferases (DNMT) 1, DNMT3A and DNMT3B via 5-Azacytidine (Aza) and 5-Aza-2"-deoxycytidine (Aza-dC) has proved to be successful toward treatment of hematologic neoplasms especially for patients with myelodysplastic syndrome. Azacitidine 89-92 DNA methyltransferase 3 beta Homo sapiens 76-82 21484930-6 2011 In particular, cancer cells harboring DNMT3B gene amplification are less sensitive to the decrease in cell viability caused by 5-azacytidine (Vidaza), 5-aza-2-deoxycytidine (Decitabine), and SGI-1027. Azacitidine 127-140 DNA methyltransferase 3 beta Homo sapiens 38-44 21229291-10 2011 Inhibiting DNMTs by 5-azacytidine (DNMT inhibitor) treatment led to significant inhibition of expression of DNMT1 and DNMT3B and enhanced expression of TSGs such as PTEN and p21 analyzed in this study. Azacitidine 20-33 DNA methyltransferase 3 beta Homo sapiens 118-124 21674861-3 2011 RESULTS: DNMT1 and DNMT3A showed statistically significant decrease of expression in 5-Aza-treated PC-MDS cells, whereas DNMT3B showed significantly decreased expression in 5-Aza-treated K562 cells. Azacitidine 173-178 DNA methyltransferase 3 beta Homo sapiens 121-127 19951990-0 2009 High DNA methyltransferase 3B expression mediates 5-aza-deoxycytidine hypersensitivity in testicular germ cell tumors. Azacitidine 50-55 DNA methyltransferase 3 beta Homo sapiens 5-29 17325427-4 2007 Inhibitors of the DNA methyltransferases DNMT1 and DNMT3b have been used in a clinical setting, these nucleotide analogues lack specificity but the side effects of low dose treatments were minimal and in 2004 Vidaza (5-azacitidine) was licensed for use in myelodysplastic syndrome. Azacitidine 217-230 DNA methyltransferase 3 beta Homo sapiens 51-57 16951151-6 2006 Oncogenic RAS increased the binding of DNMT3b to the promoter of RECK gene and this binding induced promoter methylation, which could be reversed by 5"-azacytidine and DNMT3b small interfering RNA (siRNA). Azacitidine 149-163 DNA methyltransferase 3 beta Homo sapiens 39-45 34482638-8 2022 This was associated with a dramatic increase in H3K27me3 and decrease in DNMT3B levels in 5-aza resistant cells, the exact opposite changes seen in cisplatin resistant cells. Azacitidine 90-95 DNA methyltransferase 3 beta Homo sapiens 73-79 34482638-9 2022 Evidence is presented that reciprocal regulation of polycomb and DNMT3B may be initiated by changes in DNMT3B levels as DNMT3B knockdown alone in parental cells resulted in increased expression of H3K27me3, EZH2 and BMI1, conferred 5-aza resistance and cisplatin sensitization, and mediated genome-wide repression of polycomb target gene expression. Azacitidine 232-237 DNA methyltransferase 3 beta Homo sapiens 65-71 34482638-9 2022 Evidence is presented that reciprocal regulation of polycomb and DNMT3B may be initiated by changes in DNMT3B levels as DNMT3B knockdown alone in parental cells resulted in increased expression of H3K27me3, EZH2 and BMI1, conferred 5-aza resistance and cisplatin sensitization, and mediated genome-wide repression of polycomb target gene expression. Azacitidine 232-237 DNA methyltransferase 3 beta Homo sapiens 103-109 34482638-9 2022 Evidence is presented that reciprocal regulation of polycomb and DNMT3B may be initiated by changes in DNMT3B levels as DNMT3B knockdown alone in parental cells resulted in increased expression of H3K27me3, EZH2 and BMI1, conferred 5-aza resistance and cisplatin sensitization, and mediated genome-wide repression of polycomb target gene expression. Azacitidine 232-237 DNA methyltransferase 3 beta Homo sapiens 120-126 34482638-11 2022 This study highlights that reciprocal epigenetic changes mediated by DNMT3B and polycomb may be a key driver of the unique cisplatin and 5-aza hypersensitivity of TGCTs and suggests that distinct epigenetic vulnerabilities may exist for pharmacological targeting of TGCTs. Azacitidine 137-142 DNA methyltransferase 3 beta Homo sapiens 69-75