非小细胞肺癌中的热休克蛋白——功能机制。
Heat Shock Proteins in Non-Small-Cell Lung Cancer-Functional Mechanism.
机构信息
Department of Thoracic Surgery and Institute of Thoracic Oncology, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, 610041 Chengdu, Sichuan, China.
Western China Collaborative Innovation Center for Early Diagnosis and Multidisciplinary Therapy of Lung Cancer, 610041 Chengdu, Sichuan, China.
出版信息
Front Biosci (Landmark Ed). 2023 Mar 20;28(3):56. doi: 10.31083/j.fbl2803056.
Non-small cell lung cancer (NSCLC) accounts for 80-85% of all lung cancers, which has the highest cancer-related mortality worldwide. Regardless of the therapeutic effects of chemotherapy or targeted therapy, drug resistance will occur after 1 year. Heat shock proteins (HSPs) are a class of molecular chaperones participated in protein stability and multiple intracellular signaling pathways. It has been widely reported that HSPs family is over expressed in non-small cell lung cancer, and these molecules are also associated with protein stability and multiple intracellular signaling pathways. The effect of chemotherapy drugs or targeted drugs on cancer cells is usually to induce apoptosis. It is necessary to explore the interaction between heat shock protein family and apoptosis pathway in NSCLC. Here we provide a brief review of how HSPs affect the apoptotic pathway in NSCLC.
非小细胞肺癌（NSCLC）占所有肺癌的 80-85%，是全球癌症相关性死亡率最高的癌症。无论化疗或靶向治疗的疗效如何，药物耐药性都会在 1 年后发生。热休克蛋白（HSPs）是一类参与蛋白质稳定性和多种细胞内信号通路的分子伴侣。广泛报道 HSPs 家族在非小细胞肺癌中过度表达，这些分子也与蛋白质稳定性和多种细胞内信号通路有关。化疗药物或靶向药物对癌细胞的作用通常是诱导细胞凋亡。有必要探讨热休克蛋白家族与 NSCLC 细胞凋亡途径的相互作用。本文简要综述了 HSPs 如何影响 NSCLC 中的细胞凋亡途径。
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