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miR-20b promotes growth of non-small cell lung cancer through a positive feedback loop of the Wnt/β-catenin signaling pathway

microRNAs (miRNAs or miRs) are endogenous noncoding single-stranded RNA molecules that can regulate gene expression by targeting the 3′-untranslated region and play an important role in many biological and pathological processes, such as inflammation and cancer. In this study, we found that miR-20b...

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Detalles Bibliográficos
Autores principales: Ren, Tao, Fan, Xing-Xing, Wang, Mei-Fang, Duan, Fu-Gang, Wei, Chun-Li, Li, Run-Ze, Jiang, Ze-Bo, Wang, Yu-Wei, Yao, Xiao-Jun, Chen, Ming-Wei, Tang, Yi-Jun, Leung, Elaine Lai-Han
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6959373/
https://www.ncbi.nlm.nih.gov/pubmed/31894264
http://dx.doi.org/10.3892/ijo.2019.4940
Descripción
Sumario:microRNAs (miRNAs or miRs) are endogenous noncoding single-stranded RNA molecules that can regulate gene expression by targeting the 3′-untranslated region and play an important role in many biological and pathological processes, such as inflammation and cancer. In this study, we found that miR-20b was significantly increased in human non-small cell lung cancer (NSCLC) cell lines and patient tissues, suggesting that it may possess a carcinogenic role in lung cancer. This miRNA promoted the proliferation, migration and invasion of NSCLC cells by targeting and downregulating the expression of adenomatous polyposis coli (APC), which is a negative regulator of the canonical Wnt signaling pathway. Wnt signaling activation may increase transcription of miR-20b. Therefore, miR-20b and canonical Wnt signaling were coupled through a feed-forward positive feedback loop, forming a biological regulatory circuit. Finally, an in vivo investigation further demonstrated that an increase in miR-20b promoted the growth of cancer cells. Overall, our findings offer evidence that miR-20b may contribute to the development of NSCLC by inhibiting APC via the canonical Wnt signaling pathway.