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花色苷对人胃癌 MKN28 细胞的促凋亡作用可通过增强 rudimentary 同源物增强子（ERH）增强。

Apoptotic Effects of Anthocyanins from Are Enhanced by Augmented Enhancer of the Rudimentary Homolog (ERH) in Human Gastric Carcinoma MKN28 Cells.

机构信息

Division of Basic Sciences, College of Liberal Studies, Dong-eui University, Busan 47340, Korea.

Departments of Internal Medicine, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 660-702, Korea.

出版信息

Int J Mol Sci. 2021 Mar 16;22(6):3030. doi: 10.3390/ijms22063030.

DOI:10.3390/ijms22063030
PMID:33809701
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8002340/
Abstract

Evidence suggests that augmented expression of a certain gene can influence the efficacy of targeted and conventional chemotherapies. Here, we tested whether the high expression of enhancer of the rudimentary homolog (ERH), which serves as a prognostic factor in some cancers, can influence the efficacy of anthocyanins isolated from fruits of , Meoru in Korea (AIMs) on human gastric cancer cells. The anticancer efficacy of AIMs was augmented in ERH-transfected MKN28 cells (E-MKN28 cells). Molecularly, ERH augmented AIM-induced caspase-dependent apoptosis by activating caspase-3 and -9. The ERH-augmented apoptotic effect was related to mitochondrial depolarization and inhibition of antiapoptotic proteins, XIAP, and Bcl-2. In addition, reactive oxygen species (ROS) generation was augmented in AIMs-treated E-MKN28 cells compared to AIMs-treated naïve MKN28 cells. In conclusion, ERH augmented AIM-induced caspase-dependent mitochondrial-related apoptosis in MKN28 cells. A decrease in expression of Bcl-2 and subsequent excessive ROS generation would be the mechanism for ERH-augmented mitochondrial-related apoptosis in AIMs-treated MKN28 cells. A decrease in expression of XIAP would be another mechanism for ERH-augmented caspase-dependent apoptosis in AIMs-treated MKN28 cells.

摘要

有证据表明，特定基因的增强表达可以影响靶向和常规化疗的疗效。在这里，我们测试了增强原基同源物（ERH）的高表达是否会影响从韩国梅子果实中分离出的花青素（AIMs）对人胃癌细胞的疗效，ERH 在某些癌症中是一个预后因素。AIMs 在转染 ERH 的 MKN28 细胞（E-MKN28 细胞）中的抗癌效果增强。从分子水平上讲，ERH 通过激活 caspase-3 和 -9 增强了 AIM 诱导的依赖半胱天冬酶的细胞凋亡。ERH 增强的凋亡效应与线粒体去极化和抗凋亡蛋白 XIAP 和 Bcl-2 的抑制有关。此外，与用 AIMs 处理的原始 MKN28 细胞相比，用 AIMs 处理的 E-MKN28 细胞中活性氧（ROS）的产生增加。总之，ERH 增强了 AIM 诱导的 MKN28 细胞中依赖半胱天冬酶的线粒体相关凋亡。Bcl-2 表达降低和随后 ROS 过度产生是 ERH 增强 AIM 处理的 MKN28 细胞中线粒体相关凋亡的机制。XIAP 表达降低是 ERH 增强 AIM 处理的 MKN28 细胞中依赖半胱天冬酶的凋亡的另一种机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bf/8002340/963d9eb8e18b/ijms-22-03030-g007.jpg
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