Non-small-cell lung carcinoma (NSCLC) can be classified into several subtypes, where lung squamous carcinoma (LUSC) is one common subtype. Though miR-139-3p has been reported to be implicated in the development of various cancers, its mechanisms and functions remain unclear in LUSC. In this study, miR-139-3p was screened as one of the significantly down-regulated miRNAs in LUSC by an "edgeR" differential analysis based on TCGA database, which was verified by qRT-PCR in LUSC cell lines as well. The viability and cell cycle of the LUSC cells were examined by CCK-8 and flow cytometry, respectively, exhibiting that upregulating miR-139-3p restrained cell viability and thus accelerating the cell cycle. To explain this phenomenon, we further explored the downstream target gene through miRTarBase and starBase databases, where CHEK1 was predicted as one candidate. The targeting relationship was verified by a dual luciferase assay, identifying that CHEK1 could be targeted by miR-139-3p. Then, qRT-PCR and western blot analyses were performed to detect the expression of CHEK1 mRNA and proteins under the alteration of miR-139-3p expression. Rescue experiments were conducted to confirm the impacts of miR-139-3p/CHEK1 axis on the cell viability and cell cycle of LUSC. The results indicated that the effects of miR-139-3p on the LUSC cell phenotypes could be blocked by overexpressing CHEK1. In conclusion, our study provides a novel insight into the regulatory role of miR-139-3p in the development of LUSC.
Keywords: CHEK1; DNA repair; LUSC; miR-139-3p.
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.