Problem and aim: The overexpression of MAP17 has been reported in various human carcinomas. However, its molecular mechanism in non-small cell lung cancer (NSCLC) has not been fully understood. Our study aimed to reveal the molecular mechanism of NSCLC that involved MAP17 and identify its target miRNA.
Methods: RT-qPCR and immunoblot assays were conducted to measure the expression of mRNA and protein in NSCLC tissues and cell lines. Meanwhile, the A549 cells (an NSCLC cell line) were randomly assigned to the MAP17 overexpression group, the MAP17 knockdown group and negative control group to study the roles of MAP17 in cell viability, cell proliferation, migration, invasion, and apoptosis by performing Trypan blue exclusion, MTT, colony formation, transwell, wound healing and flow-cytometric apoptosis assays. The luciferase reporter assay was conducted to confirm the target relationship between MAP17 and miR-27a-3p.
Results: The upregulation of MAP17 mRNA and protein was observed in NSCLC tissues and cell lines. In vitro, the positive roles of MAP17 on cell viability, migration, and invasion were confirmed in A549 cells. It was also found that MAP17 could inhibit cell apoptosis by suppressing the activation of the p38 pathway. This research eventually proved the target relationship between MAP17 and miR-27a-3p, and that miR-27a-3p reversed the effects of MAP17 in A549 cells by directly targeting MAP17.
Conclusions: MAP17 plays an oncogenic role in NSCLC by suppressing the activation of the p38 pathway. Apart from that, the miR-27a-3p can inhibit the expression of MAP17 to suppress the NSCLC progression.
Keywords: MAP17; Non-small cell lung cancer (NSCLC); miR-27a-3p; p38 pathway.