FAM172A modulates apoptosis and proliferation of colon cancer cells via STAT1 binding to its promoter.
FAM172A modulates apoptosis and proliferation of colon cancer cells via STAT1 binding to its promoter.
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FAM172A 通过 STAT1 与其启动子结合调节结肠癌细胞的凋亡和增殖
DOI：
10.3892/or.2015.4485
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发表时间：
2016-03
期刊：
影响因子：
4.2
通讯作者：
Liu H
中科院分区：
文献类型：
--
作者：
Qian K;Zhang J;Lu J;Liu W;Yao X;Chen Q;Lu S;Xiang G;Liu H
在我们先前的研究中，我们发现FAM172A蛋白在结肠癌组织中低表达。本研究旨在探讨FAM172A基因的功能及其转录调控机制。首先，流式细胞仪检测显示，FAM172A抑制结肠癌细胞增殖，促进细胞凋亡和分化。通过连续截断，我们确定了FAM172a的最小功能启动子区域。随后，我们发现STAT1作为一种转录因子，可以与最小的FAM172A启动子结合，这一结果通过染色质免疫沉淀(ChIP)和凝胶迁移率改变分析(EMSA)进行了鉴定。Western印迹分析和qRT-PCR结果表明，STAT1能够上调FAM172A的表达。结果表明，FAM172a能抑制结肠癌细胞的增殖，STAT1能与FAM172a最小启动子区域结合，上调FAM172a的表达。这些结果可能为深入了解FAM172a的功能及其调控机制提供依据。
In our previous study, low expression of FAM172A protein was found in colon cancer tissues. This research was planned to explore the functions of FAM172A gene and examine the mechanisms of its transcriptional regulation. Firstly, flow cytometry showed that FAM172A inhibited proliferation and promoted apoptosis and differentiation of colon cancer cells. Then through continuous truncation, we identified the minimal functional promoter region of FAM172A. Subsequently, we found that STAT1, as a transcription factor, could bind to the minimal FAM172A promoter, as evaluated using Chromatin immunoprecipitation (ChIP) and Electrophoreticmobility shift assay (EMSA). The results of Western blot analysis and qRT-PCR indicated that STAT1 was able to upregulate the expression of FAM172A. Our results showed that FAM172A could suppress proliferation of colon cancer cells, and STAT1 could bind to the minimum promoter region of FAM172A and upregulated the expression of FAM172A. These results may provide advanced insights into the functions of FAM172A and its regulatory mechanisms.