Lung cancer is the most common malignancy worldwide. Long non-coding RNA (lncRNA) p53 upregulated regulator of P53 levels (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 real-time reverse transcriptase-polymerase chain reaction (RT-qPCR). The location of PURPL was detected using RNA fluorescence in situ hybridization (FISH) assay. Protein expression was detected using western blot. Cellular functions were determined using flow cytometry. The interaction between PURPL and RNA-binding motif 4 (RBM4) was confirmed using RNA immunoprecipitation (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 cystine glutamate reverse transporter (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.

中文翻译：

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PURPL 通过调节 RBM4/xCT 信号传导促进肺癌中 M2 巨噬细胞极化

肺癌是全世界最常见的恶性肿瘤。长链非编码 RNA (lncRNA) p53 上调 P53 水平调节因子 (PURPL) 在多种癌症中异常。然而，关于其在肺癌中的作用的报道有限。本研究的目的是探讨 lncRNA PURPL 在肺癌中的潜力。使用实时逆转录酶-聚合酶链式反应 (RT-qPCR) 测定 PURPL 和 mRNA 表达。使用 RNA 荧光原位杂交 (FISH)测定法检测 PURPL 的位置。使用蛋白质印迹检测蛋白质表达。使用流式细胞术测定细胞功能。使用 RNA 免疫沉淀 (RIP) 测定证实了 PURPL 和 RNA 结合基序 4 (RBM4) 之间的相互作用。 PURPL 在肺癌细胞和患者中过度表达。过表达的 PURPL 促进 M2 巨噬细胞极化并抑制铁死亡。此外，PURPL 通过调节 RBM4 维持胱氨酸谷氨酸逆向转运蛋白 (xCT) 的 mRNA 稳定性。 xCT 敲除可拮抗过表达的 PURPL 的作用，并通过诱导巨噬细胞铁死亡来抑制 M2 巨噬细胞极化。 PURPL/RBM4/xCT 轴促进肺癌中 M2 巨噬细胞极化。因此，PURPL可能是肺癌的潜在靶点。