MS4A3 在多种癌症类型中充当肿瘤抑制因子。然而，MS4A3在肺癌中的作用仍不清楚。因此，本研究旨在探讨MS4A3在肺癌中的潜力。进行逆转录定量聚合酶链反应（RT-qPCR）以确定mRNA表达。进行CCK-8和集落形成测定以确定细胞增殖。进行管形成测定以确定血管生成。流式细胞术用于测定细胞凋亡。 JASPAR 用于分析 THAP1 的结合基序。进行荧光素酶和 ChIP 检测来验证 MS4A3 是否可以与 THAP1 相互作用从而转录灭活 EGFR。结果显示，MS4A3在非小细胞肺癌（NSCLC）患者中表达下调，这预示着NSCLC患者的临床结果较差。过表达的 MS4A3 增强 NSCLC 细胞对奥希替尼的化疗敏感性，而 MS4A3 敲低则产生相反的效果。 MS4A3 抑制 NSCLC 细胞的增殖和血管生成并促进其凋亡。此外，MS4A3 上调细胞凋亡相关的 THAP1 以使 EGFR 失活。然而，THAP1 敲低会减弱 MS4A3 的作用并促进 NSCLC 细胞的恶性行为。总之，MS4A3 在 NSCLC 中发挥抗肿瘤基因的作用。 MS4A3/THAP1/EGFR 信号传导增强肺癌对 EGFR 酪氨酸激酶抑制剂 (TKI) 的化疗敏感性。

MS4A3 functions as a tumor suppressor in multiple cancer types. However, the roles of MS4A3 in lung cancer are still unknown. Therefore, this study aims to investigate the potentials of MS4A3 in lung cancer. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was carried out to determine mRNA expression. CCK-8 and colony formation assay are conducted to determine cell proliferation. Tube formation assay is performed to determine angiogenesis. Flow cytometry is used to determine cell apoptosis. JASPAR is used to analyze the binding motif of THAP1. Luciferase and ChIP assay are conducted to verify whether MS4A3 can interact with THAP1 to transcriptionally inactivate EGFR. The results showed that MS4A3 is downregulated in non-small-cell lung cancer (NSCLC) patients, which predicts poor clinical outcomes of NSCLC patients. Overexpressed MS4A3 enhances the chemosensitivity of NSCLC cells to osimertinib, whereas MS4A3 knockdown exerts the opposite effects. MS4A3 suppresses the proliferation and angiogenesis and promotes the apoptosis of NSCLC cells. Moreover, MS4A3 upregulates apoptosis-related THAP1 to inactivate EGFR. However, THAP1 knockdown attenuates the effects of MS4A3 and promotes the malignant behavior of NSCLC cells. In conclusion, MS4A3 functions as an anti-tumor gene in NSCLC. MS4A3/THAP1/EGFR signaling enhances the chemosensitivity of lung cancer to EGFR tyrosine kinase inhibitor (TKI).