由马洛尼尔-CoA脱碳酶介导的脂肪酸氧化抑制细胞癌的进展

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Lijie Zhou^1,2, Yongbo Luo^1,2, Yuenan Liu³

¹Department of Urology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.

Cancer research

|September 20, 2023

概括

马洛尼尔-CoA脱碳酶 (MLYCD) 的下调驱动清细胞细胞癌 (ccRCC) 的进展,通过促进脂质合成. 恢复MLYCD可以增强脂肪酸氧化,抑制瘤生长,改善治疗反应.

科学领域:

在瘤学瘤学.
代谢途径代谢途径
癌症生物学癌症生物学

背景情况:

清细胞细胞癌 (ccRCC) 显示脂肪酸代谢发生显著变化,脂质储存增加促进瘤进展.
了解改变脂肪酸合成背后的分子机制对于开发有效的ccRCC疗法至关重要.

研究的目的:

调查马洛尼尔-CoA脱碳酶 (MLYCD) 在ccRCC脂肪酸代谢中的作用.
探索恢复ccRCC中MLYCD表达的治疗潜力.

主要方法:

在ccRCC患者数据中分析MLYCD表达和与预后的相关性.
在ccRCC细胞系和体内模型中对MLYCD表达的实验操纵.
评估脂肪酸合成,氧化,脂质滴积累,细胞平衡,活性氧物种和铁.
调查涉及HIF2α和eIF4G3.3的监管机制.

主要成果:

发现MLYCD在ccRCC下调,低表达与患者预后不佳相关.
恢复MLYCD表达降低了马洛尼尔-CoA水平,抑制了新脂肪酸合成,并促进了脂肪酸氧化.
通过MLYCD介导的脂肪酸氧化破坏了细胞平衡,增加了活性氧物种,并诱导了铁亡.
过度表达MLYCD抑制了瘤生长,逆转了sunitinib耐药性,并通过HIF2α介导的转化抑制来调节.

结论:

通过MLYCD介导的脂肪酸代谢对于破坏脂质平衡和抑制ccRCC进展至关重要.
激活MLYCD驱动的脂肪酸代谢是ccRCC的潜在治疗策略.

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