1. Knockdown of circular RNA VANGL1 inhibits TGF‐β‐induced epithelial‐mesenchymal transition in melanoma cells by sponging miR‐150‐5p
- Author
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Shaolong Leng, Jin Wu, Chongchao Hou, Yunsheng Xu, Laiming Mo, Xue Xie, Hongfeng Zhou, and Ling Wang
- Subjects
Epithelial-Mesenchymal Transition ,Skin Neoplasms ,Apoptosis ,Cell Movement ,Transforming Growth Factor beta ,Circular RNA ,Cell Line, Tumor ,miR-150 ,miR‐150‐5p ,melanoma ,medicine ,Humans ,circular RNA VANGL1 ,Epithelial–mesenchymal transition ,neoplasms ,Cell Proliferation ,TGF‐β ,Gene knockdown ,Chemistry ,Melanoma ,EMT ,Membrane Proteins ,RNA, Circular ,Original Articles ,Cell Biology ,medicine.disease ,Up-Regulation ,Gene Expression Regulation, Neoplastic ,MicroRNAs ,Cell culture ,Direct binding ,Cancer research ,Molecular Medicine ,RNA, Long Noncoding ,Original Article ,Carrier Proteins ,Transforming growth factor - Abstract
Melanoma is one of the most aggressive and life‐threatening skin cancers, and in this research, we aimed to explore the functional role of circular RNA VANGL1 (circVANGL1) in melanoma progression. The expression levels of circVANGL1 were observed to be significantly increased in clinical melanoma tissues and cell lines. Moreover, circVANGL1 knockdown suppressed, while circVANGL1 overexpression promoted the proliferation, migration and invasion abilities of melanoma cells. Further investigations confirmed the direct binding relation between circVANGL1 and miR‐150‐5p in melanoma, and restoration of miR‐150‐5p blocked the effects of circVANGL1 overexpression in melanoma cells. We further found that circVANGL1 was up‐regulated by TGF‐β treatment, and the enhanced EMT of TGF‐β‐treated melanoma cells was blocked by circVANGL1 knockdown. In conclusion, these results indicated that circVANGL1 might serve as a promising therapeutic target for melanoma.
- Published
- 2021