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• W2744594476 abstract "DNA methylation plays a crucial role in lots of biological processes and cancer. 5-azacytidine (5-AC), a DNA methylation inhibitor, has been used as a potential chemotherapeutic agent for cancer. In this study, we used 5-AC treatment to investigate whether DNA methylation was involved in regulation of programmed cell death (PCD) in mouse embryo fibroblast NIH-3T3 cells which could undergo PCD after treatment with TNF-α and cycloheximide (CHX). The results showed that the genomic DNA of NIH-3T3 cells was hypermethylated during PCD induced by TNF-α and CHX, and 5-AC might prevent this PCD process. However, treatment with the other three DNA methylation inhibitors, 5-aza-deoxycytidine, 6-thioguanine and RG108, did not interfere with the NIH-3T3 cell PCD process. Additionally, knockdown of DNMT1 did not affect the apoptosis process. The present results and observations indicated that 5-AC specifically inhibited the NIH-3T3 apoptosis process via a genomic DNA methylation-independent pathway. During the TNF-α and CHX-inducing apoptosis process, the PCD related BCL-2 family proteins were significantly down-regulated. Furthermore, after the small interference RNA-mediated knockdown of BCL-XL, one of the BCL-2 family proteins, 5-AC did not inhibit the apoptosis process, suggesting that 5-AC inhibited the PCD process induced by TNF-α and CHX by affecting the anti-apoptotic protein BCL-XL." @default.
• W2744594476 created "2017-08-17" @default.
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• W2744594476 date "2017-08-28" @default.
• W2744594476 modified "2023-10-18" @default.
• W2744594476 title "5‐Azacytidine specifically inhibits the NIH‐3T3 PCD process induced by TNF‐alpha and cycloheximide via affecting BCL‐XL" @default.
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• W2744594476 doi "https://doi.org/10.1002/jcb.26310" @default.
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