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作 者:邓洁[1] 罗剑波[1] 彭聪[1] 邓晓杨[1] DENG Jie;LUO Jianbo;PENG Cong(The First Affiliated Hospital of Chengdu Medical College,Chengdu,610500)
出 处:《实用癌症杂志》2021年第2期191-194,共4页The Practical Journal of Cancer
摘 要:目的研究人肉毒碱棕榈酰基转移酶1A(carnitine palmitoyltransferase 1A,CPT1A)在能量应激时(饥饿处理)卵巢癌细胞生存中的调控作用。方法①用qRT-PCR与Western Blot实验,检测能量应激对卵巢癌细胞中CPT1A表达的影响。②siRNA下调CPT1A后,用流式分析其对能量应激时卵巢癌细胞存活的影响。③siRNA下调CPT1A后,通过检测卵巢癌细胞的氧耗与ATP水平,以探讨CPT1A是否通过激活脂肪酸氧化而促进卵巢癌细胞的存活。结果①能量应激时,卵巢癌细胞中CPT1A表达在mRNA与蛋白水平均显著上调。②下调CPT1A可加重饥饿诱导的细胞凋亡。③下调CPT1A后,卵巢癌细胞中氧耗与ATP水平均显著降低,提示脂肪酸氧化被抑制。结论能量应激时CPT1A表达显著上调,进一步通过激活脂肪酸氧化而促进卵巢癌细胞的存活。Objective To investigate the regulation function of CPT1A(Carnitine Palmitoyltransferase 1A)in survival of ovarian cancer cells.Methods 1.qRT-PCR and Western Blot were employed to evaluate the effect of energy stress on the expression of CPT1A in ovarian cancer cells.2.Effect of CPT1A knockdown on proliferation of ovarian cancer cells during energy stress.3.Effect of CPT1A knockdown on oxygen consumption and ATP production of ovarian cancer cells during energy stress.Results 1.CPT1A expression was significantly up-regulated in ovarian cancer cells during energy stress.2.Knockdown of CPT1A significantly aggravated energy stress-induced ovarian cancer cell apoptosis.3.Knockdown of CPT1A significantly decreased both the consumption of oxygen and production of ATP in ovarian cancer cells during energy stress,suggesting a repressed fatty acid oxidation.Conclusion CPT1A is significantly up-regulated during energy stress,which promotes ovarian cancer survival mainly by activating fatty acid oxidation.
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