PGC1α/ CPT1A调控脂肪酸β氧化参与肿瘤放疗抵抗分子机制研究

Lipid metabolism disorder in tumor cells is not only a metabolic reprogramming strategy in the high energy demand and stress state, but also having an important correlation with tumor treatment resistance. In our previous research, we found that PGC1 alpha (peroxisome proliferator-activated receptor γ coactivator 1) and CPT1A (carnitine palmitoyl transferase) were highly activated in the radiotherapeutic resistant tumor cells. Taken the new findings as the breakthrough point, this project aims to further define PGC1 alpha/CPT1A as key molecules mediating tumor radiotherapy resistance, to activate fatty acids beta oxidation participating in cancer radiotherapy resistance. Interpretation of the function of PGC1 alpha/CPT1A in the tumor treatment resistance from the perspective of lipid metabolism and transcription regulation, will provide new scope for cancer molecular targeted therapy and important targets.

脂代谢紊乱既是肿瘤细胞在高能量需求和应激状态下的一种代谢重编程策略，同时这种代谢改变与肿瘤的治疗抗性之间具有重要相关性。本项目以肿瘤放疗抵抗细胞中高度活化的共因子PGC1α（过氧化物酶体增殖活化受体γ共活化子）及脂肪酸β氧化的关键限速酶CPT1A（肉碱棕榈酰转移酶）的新发现为切入点，进一步明确PGC1α/CPT1A作为介导肿瘤放疗抗性的关键分子，活化脂肪酸β氧化参与肿瘤放疗抵抗的作用机制。从脂代谢和转录调控的角度诠释PGC1α/CPT1A分子在肿瘤治疗抗性中的功能，将为肿瘤分子靶向治疗提供新的视角和重要靶点。

脂代谢紊乱既是肿瘤细胞在高能量需求和应激状态下的一种代谢重编程策略，同时这种代谢改变与肿瘤的治疗抗性之间具有重要相关性。本项目以肿瘤放疗抵抗细胞中高度活化的共因子PGC1α（过氧化物酶体增殖活化受体γ共活化子）及脂肪酸β氧化的关键限速酶CPT1A（肉碱棕榈酰转移酶）的新发现为切入点，进一步明确PGC1α/CEBPB/CPT1A轴作为介导肿瘤放疗抗性的关键分子，活化脂肪酸β氧化参与肿瘤放疗抵抗的作用机制。从脂代谢和转录调控的角度诠释PGC1α/CEBPB/CPT1A轴在肿瘤治疗抗性中的功能，将为肿瘤分子靶向治疗提供新的视角和重要靶点。