Chang Wei, Wang Jingjing, You Yuanqi, Wang Hongqian, Xu Shendong, Vulcano Stephen, Xu Changlu, Shen Chenlin, Li Zhi, Wang Jie
Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, School of Pharmacy, Anhui Medical University, Hefei 230032, China.
Anhui Engineering Technology Research Center of Biochemical Pharmaceuticals, Faculty of Pharmacy, Bengbu Medical College, Bengbu 233030, China.
Cancers (Basel). 2024 Jan 27;16(3):550. doi: 10.3390/cancers16030550.
Hepatocellular carcinoma (HCC), which is the third leading cause of cancer-related mortality in the world, presents a significant medical challenge. Triptolide (TP) has been identified as an effective therapeutic drug for HCC. However, its precise therapeutic mechanism is still unknown. Understanding the mechanism of action of TP against HCC is crucial for its implementation in the field of HCC treatment. We hypothesize that the anti-HCC actions of TP might be related to its modulation of HCC lipid metabolism given the crucial role that lipid metabolism plays in promoting the progression of HCC. In this work, we first demonstrate that, both in vitro and in vivo, TP significantly reduces lipid accumulation in HCC cells. Additionally, we notice that lipoprotein lipase (LPL) expression is markedly upregulated in HCC, and that its levels are positively connected with the disease's progression. It is interesting to note that TP dramatically reduces LPL activity, which in turn prevents HCC growth and reduces lipid accumulation. Additionally, the effect of TP on LPL is a direct correlation. These results definitely demonstrate that TP protects hepatocytes against abnormal accumulation of lipids by transcriptionally suppressing LPL, which reduces the development of HCC. This newly identified pathway provides insight into the process through which TP exerts its anti-HCC actions.
肝细胞癌(HCC)是全球癌症相关死亡的第三大主要原因,带来了重大的医学挑战。雷公藤甲素(TP)已被确定为治疗HCC的有效药物。然而,其确切的治疗机制仍不清楚。了解TP对HCC的作用机制对于其在HCC治疗领域的应用至关重要。鉴于脂质代谢在促进HCC进展中所起的关键作用,我们推测TP的抗HCC作用可能与其对HCC脂质代谢的调节有关。在这项工作中,我们首先证明,在体外和体内,TP均能显著降低HCC细胞中的脂质积累。此外,我们注意到脂蛋白脂肪酶(LPL)在HCC中的表达明显上调,且其水平与疾病进展呈正相关。有趣的是,TP显著降低LPL活性,进而抑制HCC生长并减少脂质积累。此外,TP对LPL的作用具有直接相关性。这些结果明确表明,TP通过转录抑制LPL保护肝细胞免受脂质异常积累的影响,从而减少HCC的发展。这一新发现的途径为TP发挥抗HCC作用的过程提供了见解。