MiR-645 promotes proliferation and migration of non-small cell lung cancer cells by targeting TP53I11.

Abstract

To research the expression and biological function of micro ribonucleic acid (miR)-645 in non-small cell lung cancer (NSCLC), and to further explore the regulatory relationship between miR-645 and tumor protein p53 inducible protein 11 (TP53I11). A total of 41 tissue samples were collected from NSCLC patients, and RNAs were extracted from these tissues and reversely transcribed. Then, the expression level of miR-645 in the 41 tissue samples of patients, as well as that in NSCLC cells and human bronchial mucosal epithelial cells, was detected by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). In vitro functional assays [methyl thiazolyl tetrazolium (MTT) assay, colony formation assay and transwell assay] were conducted to explore the effects of miR-645 on the proliferation and migration abilities of NSCLC cells. Finally, the downstream target genes of miR-645 were predicted by bioinformatics, screened via qRT-PCR and Western blotting experiments, and verified through Dual-Luciferase reporter gene assay. QRT-PCR results showed that the miR-645 expression was upregulated in the tissue samples of 35 out of 41 NSCC cases. Besides, the miR-645 expression was upregulated in NSCC cells compared with that in human bronchial mucosal epithelial cells. After interfering with miR-645 expression, in vitro functional assay (MTT assay, colony formation assay and transwell assay) results revealed that the cell proliferation, migration, and invasion were inhibited. According to the results of qRT-PCR and Western blotting, after knocking down the expression of miR-645 in NSCLC cells, the expression of TP53I11 was upregulated, and the results of Dual-Luciferase reporter gene assay confirmed that miR-645 could directly bind to TP53I11. MiR-645 expression is upregulated in NSCLC tissues and cells, and the proliferation and migration of NSCLC cells are promoted by targeted regulation on the TP53I11 expression.