Particulate matter 2.5 (PM2.5) has been implicated in lung injury and various cancers, yet its precise mechanistic role remains elusive. To elucidate the key signaling pathways underpinning PM2.5‐induced lung cancer progression, we embarked on a study examining the impact of PM2.5 both in vitro and in vivo. Lung cancer cell lines, A549 and H157, were employed for the in vitro investigations. Overexpression or knockdown techniques targeting the hnRNPA2B1 protein were implemented. Lung cancer cells were treated with a medium containing PM2.5 and subsequently prepared for in vitro evaluations. Cell growth, invasion, and migration were gauged using transwell and CCK‐8 assays. Apoptosis was ascertained through flow cytometry and western blotting of pertinent proteins. Seahorse analyses probed the influence of PM2.5 on lung cancer energy metabolism. The RNA stability assay was employed to discern the impact of PM2.5 on the stability of oxidative phosphorylation‐related genes in lung cancer. Our findings revealed that PM2.5 augmented cell proliferation, migration, and invasion rates. Similarly, a diminished apoptosis rate was observed in PM2.5‐treated cells. Elevated expression of hnRNPA2B1 was detected in lung cancer cells exposed to PM2.5. Moreover, in cells treated with PM2.5, hnRNPA2B1 knockdown markedly curtailed cell proliferation by inducing G1–S cell cycle arrest and bolstered lung cancer cell apoptosis in vitro; it also curbed xenograft tumor growth. Mechanistically, our data suggest that PM2.5 undermines the stability of mRNA transcripts associated with oxidative phosphorylation (OXPHOS) and augments the formation of processing bodies (P‐bodies), leading to an upsurge in OXPHOS levels. In conclusion, PM2.5 appears to drive lung cancer progression and migration by modulating the energy metabolism of lung cancer in a hnRNPA2B1‐dependent manner.

中文翻译：

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颗粒物 2.5 通过增加 hnRNPA2B1 的活性，延缓氧化磷酸化的 mRNA 衰减，诱导肺癌肿瘤进展

颗粒物 2.5 (PM2.5) 与肺损伤和各种癌症有关，但其精确的机制作用仍然难以捉摸。为了阐明 PM2.5 诱导肺癌进展的关键信号通路，我们开展了一项研究，考察 PM2.5 的体外和体内影响。肺癌细胞系 A549 和 H157 用于体外研究。实施了针对 hnRNPA2B1 蛋白的过表达或敲低技术。用含有 PM2.5 的培养基处理肺癌细胞，随后准备用于体外评估。使用 Transwell 和 CCK-8 检测来测量细胞生长、侵袭和迁移。通过流式细胞术和相关蛋白质的蛋白质印迹来确定细胞凋亡。Seahorse 分析探讨了 PM2.5 对肺癌能量代谢的影响。采用RNA稳定性测定来辨别PM2.5对肺癌氧化磷酸化相关基因稳定性的影响。我们的研究结果表明，PM2.5 增加了细胞增殖、迁移和侵袭率。同样，在 PM2.5 处理的细胞中观察到细胞凋亡率降低。在暴露于 PM2.5 的肺癌细胞中检测到 hnRNPA2B1 表达升高。此外，在用 PM2.5 处理的细胞中，hnRNPA2B1 敲低通过诱导 G1-S 细胞周期停滞而显着抑制细胞增殖，并在体外增强肺癌细胞凋亡。它还抑制异种移植肿瘤的生长。从机制上讲，我们的数据表明，PM2.5 破坏了与氧化磷酸化 (OXPHOS) 相关的 mRNA 转录本的稳定性，并增强了加工体 (P-体) 的形成，导致 OXPHOS 水平激增。总之，PM2.5 似乎通过以 hnRNPA2B1 依赖的方式调节肺癌的能量代谢来驱动肺癌的进展和迁移。