College of Life and Health Sciences, Institute of Biology and Medicine, Wuhan University of Science and Technology, Wuhan, Hubei, China.
Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, Tianjin, College of Biotechnology, Tianjin University of Science and Technology, Tianjin, China.
J Cell Biochem. 2020 Jun;121(5-6):3392-3405. doi: 10.1002/jcb.29613. Epub 2020 Jan 6.
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.
虽然已经开发出许多方法和新的治疗药物，但胃癌 (GC) 患者的总体生存率和长期生存率仍然不尽如人意。在这项研究中，我们研究了 microRNA miR-133a-3p 和转录因子 FOXP3 对 GC 细胞增殖和自噬的影响及其相互作用。我们的结果表明，FOXP3 的敲低增加了 GC 细胞的增殖和自噬。以前没有报道过 FOXP3 与自噬之间的关系。此外，FOXP3 可以直接结合 TP53 启动子区域并抑制其表达。miR-133a-3p 通过靶向其 3'-UTR 降低 FOXP3 的蛋白水平，从而增加增殖和自噬。我们的研究为 GC 的发展提供了新的见解，并为 GC 的临床治疗和新的药物靶点的开发提供了新的思路和理论依据。
