Microfibril-Associated Protein 2 could Regulate the Growth and Metastasis of Non-Small Cell Lung Cancer Cells via Affecting Cell Ferroptosis

Abstract

Background: Microfibril-associated protein 2 (MFAP2) plays an oncogenic role in various cancer. The purpose of study is to investigate the roles of MFAP2 in non-small cell lung cancer (NSCLC). Methods: Frist, bioinformatics were performed to determine MFAP2 expression in lung adenocarcinoma (LUAD) and Lung squamous cell carcinoma (LUSC); next, MFAP2 mRNA expression in clinical samples has been observed using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) method, and the protein expression of MFAP2 was tested using western blot and immunohistochemistry; moreover, Receiver operating characteristic (ROC) analysis has been performed to determine the potential diagnostic value of MFAP2; furthermore, A549 as well as NCI-H1299 cells were cultured, and the cell viability, proliferation, migration as well as invasion was determined by using Cell-Counting-Kit-8 (CCK-8), colony formation assay, wound healing and Matrigel assays. Finally, the effects of MFAP2 on ferroptosis of NSCLC cells were also determined by commercially available kits or western blot methods. Results: We found that the expression of MFAP2 was increased in NSCLC, and overexpression of MFAP2 predicted poor clinical outcomes. Furthermore, high levels of MFAP2 in tumor tissues can be used as a sensitive biomarker for NSCLC patients. Moreover, over-expression of MFAP2 may increase the growth and migration of NSCLC cells, and increased expression of MFAP2 also dampened Erastin-induced ferroptosis of A549 and NCI-H1299 (p < 0.001). Conclusions: In summary, MFAP2 may worked as an oncogene in NSCLC. MFAP2 deficiency suppressed the aggressiveness of NSCLC cells by increasing the ferroptosis.