The long noncoding RNA component of mitochondrial RNA-processing endoribonuclease (lncRNA RMRP) plays an important role in tumor development. In the present study, we determined the regulatory function of RMRP in non-small-cell lung cancer (NSCLC). The NSCLC tissues and the adjacent nontumor tissues were collected for the study. The RMRP expression was detected by quantitative real time-PCR in NSCLC and lung cancer cell lines. The functional validation experiments were performed to determine the role of RMRP on NSCLC progression. In addition, we identified the downstream target miRNAs for RMRP. The results showed that RMRP was elevated in NSCLC tissues and cell lines. High RMRP expression was closely associated with advanced stage for the clinical features and low overall survival in NSCLC patients. Functional assay showed that loss of RMRP markedly inhibited cell proliferation, migration, and invasion. Flow cytometry assay demonstrated that the inhibition of RMRP dramatically induced cell cycle arrest in the G0/G1 phase. Moreover, we found that the role of RMRP on NSCLC cell progression was modulated by the inhibition of miR-1-3p. Collectively, our results demonstrated that the "RMRP-miR-1-3p" axis might promote NSCLC progression. Hence, these investigations will provide a therapeutic target and strategy for the treatment of NSCLC progression.
Keywords: RNA component of mitochondrial RNA processing (RMRP); cell cycle arrest; miR-1-3p; non-small cell lung cancer.
© 2019 Wiley Periodicals, Inc.