PURPL promotes M2 macrophage polarization in lung cancer via regulating RBM4/xCT signaling

Abstract

Lung cancer is the most common malignancy worldwide. Long non-coding RNA (lncRNA) PURPL is abnormally in various cancers. However, the reports on its roles in lung cancer are limited. The purpose of present study is to investigate the potentials of lncRNA PURPL in lung cancer. PURPL and mRNA expression was determined using RT-qPCR. The location of PURPL was detected using RNA FISH assay. Protein expression was detected using western blot. Cellular functions were determined using flow cytometry. The interaction between PURPL and RBM4 was confirmed using RIP assay. PURPL was overexpressed in lung cancer cells and patients. Overexpressed PURPL promoted M2 macrophage polarization and suppressed ferroptosis. Additionally, PURPL maintained the mRNA stability of xCT via regulating RBM4. xCT knockdown antagonized the effects of overexpressed PURPL and inhibited M2 macrophage polarization via inducing macrophage ferroptosis. PURPL/RBM4/xCT axis promoted M2 macrophage polarization in lung cancer. Therefore, PURPL may be a potential target of lung cancer.