三大营养物质代谢重编程及其在胰腺癌耐药机制中的研究进展  

Metabolic Reprogramming of Three Nutrients and Their Roles in Drug Resistance Mechanism in Pancreatic Cancer

作　　者：杨帆 武晓慧[1] Yang Fan;Wu Xiaohui(Clinical Medical College,Xi'an Medical University,Xi’an 710021,China)

机构地区：[1]西安医学院临床医学院,西安710021

出　　处：《中国药师》2021年第12期2237-2243,共7页China Pharmacist

基　　金：2019年陕西省省级大学生创新创业训练计划项目(编号:S201911840032);西安医学院2019年校级大学生创新创业训练计划项目(编号:121519056);中尼友好拉吉姆医学实验室开放基金(编号:18LJM02);西安医学院博士启动基金项目(编号:2020DOC04)。

摘　　要：胰腺癌是一种恶性程度极高的肿瘤,5年生存率不足10%,外科根治性手术与化学治疗是主要的治疗手段。胰腺癌现有化疗药物的效果有限,近年来以吉西他滨为基础的化疗方案的耐药现象越来越多见。胰腺癌中存在葡萄糖、脂质、氨基酸等营养物质代谢重编程现象,在肿瘤细胞的增殖、进展与耐药机制中发挥重要作用。本文系统地回顾近年来胰腺癌的糖、脂及氨基酸3个方面代谢重编程现象及其与胰腺癌耐药关系的研究进展,以期为新的胰腺癌化疗药物的开发及解决耐药提供理论参考。Pancreatic cancer is a highly malignant tumor with 5-year survival rate less than 10%. In recent years, the drug resistance of gemcitabine-based chemotherapy is more and more common. Metabolic reprogramming of glucose, lipids and amino acids in pancreatic cancer plays important roles in the proliferation, progression and drug resistance of tumor cells. The recent advances in metabolic reprogramming of glucose, lipid and amino acids in pancreatic cancer and their relationships with drug resistance were systematically reviewed in this article in order to provide theoretical reference of new chemotherapeutic drugs for pancreatic cancer and solving the problem of drug resistance.

关 键 词：胰腺癌 代谢重编程 耐药 

分 类 号：R735.9[医药卫生—肿瘤]