BACKGROUND: Colon cancer is the third leading cause of tumor-related deaths in the world. Inhibition of autophagy in the treatment of malignant tumors has attracted extensive attention. However, the association between inhibition of autophagy by 3-methyladenine (3-MA) and epithelial mesenchymal transformation (EMT) in colon cancer cells has not yet been fully elucidated. METHODS: In this study, colon cancer cell lines (LOVO and SW620) were treated with 3-MA. Wound healing assays and transwell assays were used to detect the effect of inhibition of autophagy on the migration and invasion of colon cancer cells. The expression of EMT-associated markers, Twist1, E-cadherin, and vimentin, in colon cancer cells with and without 3-MA treatment was detected by Western blotting, immunohistochemistry, immunofluorescence staining, and real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). RESULTS: Our data showed that inhibition of autophagy by 3-MA significantly enhanced the migration and invasion of colon cancer cells. At the molecular level, inhibition of autophagy upregulated the expression of Twist1 and vimentin, downregulated the expression of E-cadherin, and induced the EMT of colon cancer cells. CONCLUSIONS: Inhibition of autophagy by 3-MA upregulated the expression of Twist1 in colon cancer cells and promoted cancer cell migration and invasion through EMT. Inhibition of autophagy may have adverse effects on colon cancer.
Inhibition of autophagy by 3-methyladenine promotes migration and invasion of colon cancer cells through epithelial mesenchymal transformation.
3-甲基腺嘌呤通过抑制自噬促进结肠癌细胞通过上皮间质转化而迁移和侵袭
阅读:4
作者:Zhang Xiaoyang, Wang Hui, Yu Miao, Ma Kun, Ning Li
| 期刊: | Translational Cancer Research | 影响因子: | 1.700 |
| 时间: | 2022 | 起止号: | 2022 Aug;11(8):2834-2842 |
| doi: | 10.21037/tcr-22-1736 | 研究方向: | 细胞生物学 |
| 疾病类型: | 肠癌 | ||
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
