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GDH1抑制剂R162靶向EGFR通路抑制NSCLC细胞的增殖

邬爱红, 韩田雨, 许飞*

摘要

在我国恶性肿瘤中，肺癌的发病率及死亡率位居首位，其中非小细胞肺癌（NSCLC）占比可达80%-85%。近年来，肿瘤代谢重编程成为癌症研究的热点领域，谷氨酰胺代谢增强是肿瘤代谢的主要特征之一。谷氨酸脱氢酶GDH1是谷氨酰胺代谢的关键酶，在多种肿瘤中发挥促癌作用，是目前抗肿瘤药物研发的潜在靶点。R162是GDH1的特异性小分子抑制剂，在NSCLC中的作用研究较少，部分研究仅探讨了R162对NSCLC细胞转移的影响，而R162是否影响NSCLC细胞的增殖尚未知晓。本研究证明了R162抑制NSCLC细胞的增殖和细胞周期运转，阐明了R162抑制NSCLC细胞的EGFR信号通路来抑制细胞增殖，还揭示了R162诱导NSCLC的线粒体自噬。综上所述，我们的研究阐明了R162对NSCLC细胞的影响及其机制，对以R162为基础开发新型肺癌治疗药物提供了理论依据。

关键词

谷氨酸脱氢酶1；R162；表皮生长因子受体；细胞周期；非小细胞肺癌细胞

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参考

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