Epigenetic silencing of TPM2 contributes to colorectal cancer progression upon RhoA activation
Epigenetic silencing of TPM2 contributes to colorectal cancer progression upon RhoA activation
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TPM2 的表观遗传沉默有助于 RhoA 激活后结直肠癌的进展
DOI：
10.1007/s13277-016-5103-1
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发表时间：
2016-09-01
期刊：
影响因子：
--
通讯作者：
Wang, Jianping
中科院分区：
文献类型：
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作者：
Cui, Ji;Cai, Yonghua;Wang, Jianping
Beta-tropomyosin (beta-tropomyosin, TPM2) has been found to be downregulated in colorectal cancer (CRC) in previous studies. In this study, we aimed to investigate the mechanisms and potential biological consequences of the downregulation of TPM2 in colorectal cancer. TPM2 expression in colorectal cancer was assessed by qRT-PCR and immunostaining. The biological functions of TPM2 were assessed in cell lines either overexpressing or underexpressingTPM2. Aberrant DNA methylation in the promoter region is associated with suppression of TPM2 expression in primary colorectal cancer tissue samples. Treatment with the demethylation agent 5-AZA can induceTPM2 expression in colorectal cancer cell lines. Reconstitution of TPM2 suppresses cell proliferation and migration in colorectal cancer cell lines, whereas the loss of TPM2 expression is associated with increased tumor proliferation and migration in vitro, which was accompanied by RhoA activation. In summary, our findings indicate that TPM2 appears to be commonly silenced by aberrant DNA methylation in colon cancer. TPM2 loss is associated with RhoA activation and tumor proliferation.
