首页|脂质代谢重编程对非小细胞肺癌表皮生长因子受体-酪氨酸激酶抑制剂耐药影响的研究进展

脂质代谢重编程对非小细胞肺癌表皮生长因子受体-酪氨酸激酶抑制剂耐药影响的研究进展

Progress on the impact of lipid metabolism reprogramming on resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer

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非小细胞肺癌(NSCLC)是肺癌中的主要类型,占比85%~90%.表皮生长因子受体-酪氨酸激酶抑制剂(EGFR-TKIs)的使用极大改善了 NSCLC患者的预后.然而,随着药物使用时间的延长会不可避免地出现获得性耐药,从而导致疾病的复发、进展、甚至患者的死亡.代谢重编程是恶性肿瘤的标志之一,是指肿瘤细胞为满足能量需求而发生代谢改变.在多种癌症中,肿瘤细胞的脂质合成、分布以及分解代谢发生了改变,以适应肿瘤微环境中营养、氧气匮乏的特点.本文主要关注NSCLC中,脂质代谢重编程如何导致EGFR-TKIs的耐药以及如何通过调节脂质代谢增加NSCLC对于EGFR-TKIs的敏感性,归纳并总结现有的研究进展,以期为EGFR-TKIs耐药相关基础研究及临床治疗提供参考.
Non-small cell lung cancer(NSCLC)is the main type of lung cancer,accounting for 85%to 90%of cases.The use of epidermal growth factor receptor tyrosine kinase inhibitors(EGFR-TKIs)has greatly improved the prognosis of NSCLC patients.However,with prolonged drug use,the inevitable occurrence of acquired resistance leads to disease recurrence,progression,and even patient's death.Metabolic reprogramming is one of the hallmarks of malignant tumors and refers to metabolic changes in tumor cells to meet energy needs.In various cancers,lipid synthesis,distribution,and catabolism of tumor cells are altered to adapt to the lack of nutrients and oxygen in the tumor microenvironment.This paper focuses on how lipid metabolism reprogramming in NSCLC leads to resistance to EGFR-TKIs and how modulation of lipid metabolism increases the sensitivity of NSCLC to EGFR-TKIs.It summarizes and consolidates existing research progress to provide a reference for basic research and clinical treatment of EGFR-TKIs resistance in NSCLC.

Non-small cell lung cancerLipid metabolism reprogrammingEpidermal growth factor receptor tyrosine kinase inhibitorsResistanceStatins

肖辛瑶、郭舜尧、陆海艳、沈华

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南京医科大学附属逸夫医院肿瘤科,江苏南京 211100

非小细胞肺癌 脂质代谢重编程 表皮生长因子受体-酪氨酸激酶抑制剂 耐药 他汀类药物

2024

中国临床研究
中华预防医学会

中国临床研究

CSTPCD
影响因子:0.943
ISSN:1674-8182
年,卷(期):2024.37(1)
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