miR-133a-3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer
miR-133a-3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer
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MiR-133a-3p/FOXP3轴调节胃癌细胞增殖和自噬
DOI：
10.1002/jcb.29613
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发表时间：
2020-01-06
影响因子：
4
通讯作者：
Zhang, Tong-Cun
中科院分区：
文献类型：
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作者：
Li, Jia-Peng;Zhang, Hui-Min;Zhang, Tong-Cun
虽然开发了许多方法和新的治疗药物，但胃癌（GC）患者的总生存率和长期生存率仍不令人满意。在本研究中，我们研究了microRNA miR-133a-3p和转录因子FOXP3对胃癌细胞增殖和自噬的影响及其相互作用。我们的研究结果表明，FOXP3的敲低增加了GC细胞的增殖和自噬。FOXP3与自噬的关系此前未见报道。此外，FOXP3可以直接结合TP53的启动子区域，抑制其表达。miR-133a-3p通过靶向FOXP3的3′-UTR，降低FOXP3的蛋白水平，从而促进细胞增殖和自噬。我们的研究为GC的发展提供了新的见解，为GC的临床治疗和新药靶点的开发提供了新的思路和理论依据。
Although many methods and new therapeutic drugs have been developed, the overall survival rate and long-term survival rate of patients with gastric cancer (GC) are still not satisfactory. In this study, we investigated the effects of microRNA miR-133a-3p and transcription factor FOXP3 on proliferation and autophagy of GC cells and their interactions. Our results showed that knockdown of FOXP3 increased the proliferation and autophagy of GC cells. The relationship between FOXP3 and autophagy has not been reported previously. In addition, FOXP3 could directly bind the promoter region of TP53 and inhibit its expression. miR-133a-3p increased the proliferation and autophagy via decreasing the protein level of FOXP3 by targeting its 3 '-UTR. Our research provides new insights into the development of GC and provides new ideas and theoretical basis for the clinical treatment of GC and the development of new drug targets.