力达霉素通过调节 Mfn2 的表达诱导胰腺癌细胞发生线粒体自噬。
Lidamycin induces mitophagy in pancreatic cancer cells by regulating the expression of Mfn2.
机构信息
Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases, School of Basic Medical Sciences, North China University of Science and Technology, Tangshan, Hebei, China.
College of Life Sciences, North China University of Science and Technology, 21 Bohai Road, Caofeidian Xincheng, Tangshan, Hebei, China.
出版信息
Sci Rep. 2024 Sep 5;14(1):20713. doi: 10.1038/s41598-024-71377-4.
Lidamycin (LDM) has been confirmed to have a strong anti-pancreatic cancer effect and can affect the mitochondrial function of pancreatic cancer cells. Mitofusin-2 (Mfn2) is located in the outer membrane of mitochondria, and Mfn2 is currently believed to play a role in cancer inhibition in pancreatic cancer. In order to explore whether the anti-pancreatic cancer effect of LDM is related to Mfn2-mediated mitophagy, Bioinformatics and in vitro cell experiments are used for experimental research. The experimental results demonstrated that Mfn2 is correlated with mitochondrial autophagy in pancreatic cancer. Lidamycin can increase the expression of Mfn2 in pancreatic cancer and affect the process of EMT, affect the level of reactive oxygen species and mitochondrial membrane potential, and increase the expression of mitochondrial autophagy marker proteins BNIP3L and Beclin1. These results demonstrate that Mfn2 affects mitophagy in pancreatic cancer cells by regulating the expression of Mfn2.
力达霉素（LDM）已被证实具有较强的抗胰腺癌作用，可影响胰腺癌细胞的线粒体功能。线粒体融合蛋白 2（Mfn2）位于线粒体的外膜上，目前认为 Mfn2 在胰腺癌的抑癌作用中发挥作用。为了探讨 LDM 的抗胰腺癌作用是否与 Mfn2 介导的线粒体自噬有关，采用生物信息学和体外细胞实验进行实验研究。实验结果表明，Mfn2 与胰腺癌中的线粒体自噬相关。力达霉素可增加胰腺癌中 Mfn2 的表达，并影响 EMT 过程，影响活性氧和线粒体膜电位水平，增加线粒体自噬标记蛋白 BNIP3L 和 Beclin1 的表达。这些结果表明，Mfn2 通过调节 Mfn2 的表达来影响胰腺癌细胞中的线粒体自噬。
Zotero 插件