Literature DB >> 19661336

Methylation mediated silencing of TMS1 in breast cancer and its potential contribution to docetaxel cytotoxicity.

Edna Gordian1, Kavitha Ramachandran, Rakesh Singal.   

Abstract

BACKGROUND: The tumor suppressor gene TMS1 (target of methylation-induced silencing) has been described in the literature as a pro-apoptotic gene. This study examined the methylation status of TMS1 in breast cancer cells and its potential role in sensitivity to docetaxel chemotherapy.
MATERIALS AND METHODS: Methylation of the TMS1 promoter was examined by methylation-specific PCR (MS-PCR) and gene expression was analyzed by reverse transcriptase PCR (RT-PCR). Apoptosis was evaluated by annexin V/propidium iodide staining followed by flow cytometric analysis. RESULTS AND
CONCLUSION: The TMS1 promoter was unmethylated in ZR75-1, MB-231 and MCF7 cells which expressed the gene and partially methylated in SKBR3 and Hs578t cells in which TMS1 expression was down-regulated. Treatment of SKBR3 and Hs578t cells with demethylating agents resulted in reactivation of the TMS1 gene. Pretreatment with 5-azacytidine increased sensitivity to docetaxel treatment in SKBR3 and Hs578t cells, indicating that TMS1 reactivation in these cells may contribute to docetaxel sensitivity.

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Year:  2009        PMID: 19661336

Source DB:  PubMed          Journal:  Anticancer Res        ISSN: 0250-7005            Impact factor:   2.480


  8 in total

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Journal:  Cancer Discov       Date:  2013-08-16       Impact factor: 39.397

Review 2.  Comprehensive review of ASC structure and function in immune homeostasis and disease.

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Journal:  Mol Biol Rep       Date:  2020-03-02       Impact factor: 2.316

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Review 4.  Epigenetics in the development, modification, and prevention of cardiovascular disease.

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Authors:  Hui Miao; Linlin Wang; Haomiao Zhan; Jiangshan Dai; Yanbo Chang; Fan Wu; Tao Liu; Zhongyu Liu; Chunfang Gao; Ling Li; Xu Song
Journal:  PLoS Genet       Date:  2019-05-14       Impact factor: 5.917

  8 in total

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