miR-133a-3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

被引:35
|
作者
Li, Jia-Peng [1 ]
Zhang, Hui-Min [1 ]
Liu, Mei-Jun [1 ]
Xiang, Yuan [1 ]
Li, Hui [1 ]
Huang, Feng [1 ]
Li, Han-Han [1 ]
Dai, Zhou-Tong [1 ]
Gu, Chao Jiang [1 ]
Liao, Xing-Hua [1 ]
Zhang, Tong-Cun [1 ,2 ]
机构
[1] Wuhan Univ Sci & Technol, Coll Life & Hlth Sci, Inst Biol & Med, Wuhan 430081, Hubei, Peoples R China
[2] Tianjin Univ Sci & Technol, Coll Biotechnol, Minist Educ, Key Lab Ind Fermentat Microbiol, Tianjin, Peoples R China
基金
中国国家自然科学基金;
关键词
autophagy; FOXP3; gastric cancer; miR-133a-3p; proliferation; FOXP3; EXPRESSION; DOWN-REGULATION; IMMUNE ESCAPE; T-CELL; MIRNA; INVASION; MIGRATION; THERAPEUTICS; ASSOCIATION; PROGRESSION;
D O I
10.1002/jcb.29613
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:3392 / 3405
页数:14
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