CircRNF20 aggravates the progression of non-small-cell lung carcinoma by activating MAPK9.

Abstract

To explore the clinical significance of circRNF20 in non-small-cell lung carcinoma (NSCLC), and its regulatory effects on NSCLC cell functions by activating MAPK9. Relative levels of circRNF20 and MAPK9 in NSCLC tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between circRNF20, MAPK9 and pathological factors in NSCLC patients was analyzed. Prognostic potentials of circRNF20 and MAPK9 in NSCLC were assessed by Kaplan-Meier method. The interaction between circRNF20 and MAPK9 was tested by Dual-Luciferase reporter assay. Regulatory effects of circRNF20 and MAPK9 on proliferative abilities in H358 and SPC-A1 cells were examined by Cell Counting Kit-8 (CCK-8) and colony formation assay. CircRNF20 and MAPK9 were upregulated in NSCLC tissues than normal ones. They were correlated to T stage and poor prognosis in NSCLC patients, while their levels were unrelated to gender, age, and incidences of lymphatic and distant metastasis. Knockdown of circRNF20 attenuated proliferative abilities in H358 and SPC-A1 cells. On the contrary, the overexpression of MAPK9 yielded the opposite results. MAPK9 was the target gene binding circRNF20, which was able to reverse the regulatory effect of circRNF20 on NSCLC proliferation. CircRNF20 and MAPK9 are upregulated in NSCLC cases, which are closely linked to T stage in NSCLC patients. They are independent prognostic factors for NSCLC. By activating MAPK9, circRNF20 stimulates NSCLC proliferation.