Non-small cell lung cancer (NSCLC) encompasses approximately 85% of all lung cancer cases and is the foremost cancer type worldwide; it is prevalent in both sexes and known for its high fatality rate. Expanding scientific inquiry underscores the indispensability of microRNAs in NSCLC. Here, we probed the impact of miR-873-5p on NSCLC development and chemoresistance. qRT‒PCR was used to measure the miR-873-5p level in NSCLC cells with or without chemoresistance. A model of miR-873-5p overexpression was constructed. The proliferation and viability of NSCLC cells were evaluated through CCK8 and colony formation experiments. Cell migration and invasion were monitored via Transwell assays. Western blotting was used to determine the levels of YWHAE, PI3K, AKT, EMT, apoptosis, and autophagy-related proteins. The sensitivity of NSCLC cells to the chemotherapeutic agent gefitinib was assessed. Additionally, the correlation of YWHAE with miR-873-5p was validated via a dual-luciferase reporter assay and RNA immunoprecipitation (RIP). Overexpressed miR-873-5p suppressed migration, proliferation, invasion, and EMT while concurrently stimulating apoptotic processes. miR-873-5p was downregulated in NSCLC cells resistant to gefitinib. Upregulating miR-873-5p reversed gefitinib resistance by inducing autophagy. YWHAE was confirmed to be a downstream target of miR-873-5p. YWHAE overexpression promoted the malignant behaviors of NSCLC cells and boosted tumor growth, while these effects were reversed following miR-873-5p overexpression. Subsequent investigations revealed that overexpressing YWHAE promoted PI3K/AKT pathway activation, with miR-873-5p displaying inhibitory effects on the YWHAE-mediated PI3K/AKT signaling cascade. miR-873-5p affects proliferation, invasion, migration, EMT, autophagy, and chemoresistance in NSCLC by controlling the YWHAE/PI3K/AKT axis.

非小细胞肺癌 (NSCLC) 约占所有肺癌病例的 85%，是全球最重要的癌症类型；它在男女中都很流行，并以其高死亡率而闻名。不断扩大的科学研究强调了 microRNA 在 NSCLC 中的重要性。在这里，我们探讨了 miR-873-5p 对 NSCLC 发展和化疗耐药的影响。 qRT-PCR 用于测量具有或不具有化疗耐药性的 NSCLC 细胞中 miR-873-5p 的水平。构建了miR-873-5p过表达模型。通过CCK8和集落形成实验评估NSCLC细胞的增殖和活力。通过 Transwell 检测监测细胞迁移和侵袭。 Western blotting用于测定YWHAE、PI3K、AKT、EMT、细胞凋亡和自噬相关蛋白的水平。评估了 NSCLC 细胞对化疗药物吉非替尼的敏感性。此外，通过双荧光素酶报告基因测定和 RNA 免疫沉淀 (RIP) 验证了 YWHAE 与 miR-873-5p 的相关性。过表达的 miR-873-5p 抑制迁移、增殖、侵袭和 EMT，同时刺激细胞凋亡过程。 miR-873-5p 在吉非替尼耐药的 NSCLC 细胞中下调。上调 miR-873-5p 通过诱导自噬逆转吉非替尼耐药。 YWHAE 被证实是 miR-873-5p 的下游靶标。 YWHAE 过表达促进 NSCLC 细胞的恶性行为并促进肿瘤生长，而这些效应在 miR-873-5p 过表达后逆转。随后的研究表明，过表达 YWHAE 促进 PI3K/AKT 通路激活，而 miR-873-5p 对 YWHAE 介导的 PI3K/AKT 信号级联显示出抑制作用。 miR-873-5p 通过控制 YWHAE/PI3K/AKT 轴影响 NSCLC 中的增殖、侵袭、迁移、EMT、自噬和化疗耐药。