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首页> 外文期刊>Journal of Cellular Physiology >miR-203 Is a Direct Transcriptional Target of E2F1 and Causes G1 Arrest in Esophageal Cancer Cells
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miR-203 Is a Direct Transcriptional Target of E2F1 and Causes G1 Arrest in Esophageal Cancer Cells

机译：mir - 203直接转录E2F1的目标和导致食道癌细胞G1逮捕

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摘要

miR-203 act as tumor repressor by inhibiting cell proliferation and is repressed in a variety of human tumors, although the molecular mechanisms responsible have not been elucidated. Here, we reveal that miR-203 is regulated by E2F1, an important transcription factor that can induce cell proliferation by controlling cell cycle progression. We found that miR-203 expression was induced by cisplatin, which also induced E2F1 protein accumulation in esophageal squamous cell carcinoma (ESCC) cell lines. miR-203 expression was elevated upon activation of ectopic E2F1, whereas this induction was abolished when the E2F1 gene was silenced. Moreover, with luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays, we demonstrated that E2F1 transactivates miR-203 by directly binding to the miR-203 gene promoter. In addition, we found that miR-203 inhibited cell proliferation by inducing G1/S cell cycle arrest, but not apoptosis, in ESCC cell lines. Finally, we observed that miR-203 negatively inhibited the expression of CDK6, subsequently decreasing E2F1 expression possibly through Rb phosphorylation. Taken together, our data show that cancer-related miR-203 is a novel transcriptional target of E2F1 and that it regulates cell cycle arrest by participating in a feedback loop with E2F1. (C) 2014 Wiley Periodicals, Inc.
机译：mir - 203作为肿瘤抑制因子通过抑制细胞扩散和在各种各样的压抑人类肿瘤,虽然分子机制负责尚未阐明。显示,mir - 203由E2F1监管,一个重要的转录因子,可以诱发通过控制细胞周期细胞增殖进展。顺铂诱导,诱导E2F1在食管鳞状细胞蛋白质积累癌(ESCC)细胞系。是异位E2F1激活后,而这个感应时被废除E2F1基因沉默。记者化验和染色质免疫沉淀反应(芯片)分析,我们证明了E2F1通过直接绑定到transactivates mir - 203mir - 203基因启动子。mir - 203抑制细胞增殖,诱导G1 / S细胞周期阻滞,但不是细胞凋亡ESCC细胞系。mir - 203消极抑制的表达CDK6,随后减少E2F1表达式可能通过Rb磷酸化。在一起,我们的数据显示,癌症相关mir - 203是一种新型转录E2F1的目标,并调节细胞周期阻滞参与E2F1的反馈回路。2014年威利期刊、公司。

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