...
首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Methylation-mediated silencing of TMS1 in pancreatic cancer and its potential contribution to chemosensitivity.
【24h】

Methylation-mediated silencing of TMS1 in pancreatic cancer and its potential contribution to chemosensitivity.

机译:甲基化介导的TMS1在胰腺癌中的沉默及其对化学敏感性的潜在贡献。

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

BACKGROUND: Resistance to chemotherapeutic agents, resulting in part from epigenetic silencing of pro-apoptotic genes, is one of the causes of treatment failure of pancreatic cancer. We examined whether epigenetic silencing of target of methylation induced silencing 1 (TMS1) contributes to resistance to chemotherapy in pancreatic cancer. MATERIALS AND METHODS: Methylation analysis was performed by methylation-specific PCR (MS-PCR) and gene expression was analyzed by quantitative reverse transcriptase PCR (qRT-PCR). MIA PaCa-2 cells were transfected with pCMV6-XL5/TMS1 plasmid and the effect of TMS1 expression on sensitivity to gemcitabine and docetaxel was determined. Cell viability was measured using Cell Titer Blue assay. RESULTS: TMS1 expression was repressed in MIA PaCa-2 cells by DNA methylation. Up-regulation of TMS1 by recombinant gene expression in MIA PaCa-2 cells or by pre-treatment of these cells with 5-azacytidine resulted in enhanced sensitivity to gemcitabine and docetaxel. CONCLUSION: Our results suggest that TMS1 is a potential therapeutic target in pancreatic cancer.
机译:背景:对化学治疗药物的抗性,部分是由于促凋亡基因的表观遗传沉默所致,是胰腺癌治疗失败的原因之一。我们检查了甲基化诱导的沉默1(TMS1)的目标的表观遗传沉默是否有助于对胰腺癌的化疗耐药。材料与方法:通过甲基化特异性PCR(MS-PCR)进行甲基化分析,并通过定量逆转录酶PCR(qRT-PCR)分析基因表达。用pCMV6-XL5 / TMS1质粒转染MIA PaCa-2细胞,并测定TMS1表达对吉西他滨和多西他赛敏感性的影响。使用细胞滴度蓝测定法测量细胞活力。结果:通过DNA甲基化抑制了MIA PaCa-2细胞中TMS1的表达。通过在MIA PaCa-2细胞中重组基因表达或通过用5-氮杂胞苷预处理这些细胞,可以上调TMS1对吉西他滨和多西他赛的敏感性。结论:我们的结果表明TMS1是胰腺癌的潜在治疗靶标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号