Metastasis is a major cause of death in lung cancer. The aim of this study is to analyze the role and mechanism of PI3K catalytic subunit gamma (PIK3CG, also known as p110γ) in lung cancer cell migration and metastasis. Knockdown (KD) and overexpression (OE) of PIK3CG expression in lung cancer cell lines A549 and H1299 in vitro cultured was achieved. Two PIK3CG-specific inhibitors, Eganelisib and CAY10505, were used to treat A549 and H1299 cells. An experimental lung metastasis mouse model was constructed using tail vein injection of LLC cells. Finally, a co-culture system was established using Transwell chambers. Compared with the NC group, the number of cells that completed migration and the expression levels of matrix metalloproteinases (MMPs) were significantly reduced in the KD group and Eganelisib and CAY10505 treatment groups, while the number of cells that migrated successfully and the expression levels of MMPs were significantly increased in the OE group. Lung tissues of mice injected with PIK3CG-stabilized overexpressed LLC cells showed more pronounced lung cancer growth, lung metastatic nodules, neutrophil infiltration and MMPs expression. Co-culture with neutrophils, soluble extracts of neutrophils and cathepsin G all promoted the migration of lung cancer cells. PIK3CG overexpression in tumor cells significantly promoted the migration and metastasis of lung cancer cell.

转移是肺癌死亡的主要原因。本研究旨在分析PI3K催化亚基γ（PIK3CG，又称p110γ）在肺癌细胞迁移和转移中的作用和机制。在体外培养的肺癌细胞系A549和H1299中实现了PIK3CG表达的敲低（KD）和过表达（OE）。两种 PIK3CG 特异性抑制剂 Eganelisib 和 CAY10505 用于处理 A549 和 H1299 细胞。采用尾静脉注射LLC细胞构建实验性肺转移小鼠模型。最后，使用Transwell小室建立了共培养系统。与NC组相比，KD组、Eganelisib和CAY10505治疗组完成迁移的细胞数和基质金属蛋白酶（MMPs）的表达水平显着减少，而迁移成功的细胞数和基质金属蛋白酶（MMPs）的表达水平显着降低。 OE 组的 MMP 显着增加。注射 PIK3CG 稳定的过表达 LLC 细胞的小鼠肺组织显示出更明显的肺癌生长、肺转移结节、中性粒细胞浸润和 MMP 表达。与中性粒细胞、中性粒细胞可溶性提取物和组织蛋白酶G共培养均促进肺癌细胞的迁移。肿瘤细胞中PIK3CG过表达显着促进肺癌细胞的迁移和转移。