Resveratrol induces human colorectal cancer cell apoptosis by activating the mitochondrial pathway via increasing reactive oxygen species
Resveratrol induces human colorectal cancer cell apoptosis by activating the mitochondrial pathway via increasing reactive oxygen species
复制标题
白藜芦醇通过增加活性氧激活线粒体途径诱导人结直肠癌细胞凋亡
DOI：
10.3892/mmr.2020.11809
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发表时间：
2021-03-01
影响因子：
3.4
通讯作者：
Zhang, Qingling
中科院分区：
文献类型：
--
作者：
Fu, Yun;Ye, Yuedian;Zhang, Qingling
根据 2018 年全球癌症统计，结直肠癌 (CRC) 是全球第三大最常见的恶性肿瘤，也是癌症相关死亡的第二大原因。白藜芦醇 (RSV) 是一种酚类化合物，对包括乳腺癌和胃癌在内的多种癌症具有抗癌作用。然而，RSV 在 CRC 中的功能和机制尚不完全清楚。本研究旨在通过 Cell Counting Kit-8、细胞凋亡、活性氧 (ROS) 和蛋白质印迹分析来研究 RSV 在 CRC 细胞中的抗癌作用和机制。结果表明，与对照组相比，RSV 剂量依赖性地抑制 CRC 细胞活力，并增加细胞凋亡和 ROS 水平。与对照细胞相比，RSV处理的CRC细胞中Bax、细胞色素c、cleaved caspase-9和cleaved caspase-3的蛋白表达水平上调，而Bcl-2表达水平下调。结果表明，RSV可能通过增加ROS释放来激活线粒体凋亡途径。目前的研究表明，RSV 通过调节 ROS 介导的线粒体凋亡途径而具有针对 CRC 的抗肿瘤活性。
Colorectal cancer (CRC) is the third most commonly diagnosed malignancy and the second leading cause of cancer-related mortality worldwide according to Global Cancer Statistics 2018. Resveratrol (RSV) is a phenolic compound that possesses anticancer functions against various types of cancer, including breast and gastric cancer. However, the functions and mechanism underlying RSV in CRC are not completely understood. The present study aimed to investigate the anticancer effects and mechanism underlying RSV in CRC cells by conducting Cell Counting Kit-8, apoptosis, reactive oxygen species (ROS) and western blotting assays. The results suggested that RSV dose-dependently inhibited CRC cell viability, and increased cell apoptosis and ROS levels compared with the control group. The protein expression levels of Bax, cytochrome c, cleaved caspase-9 and cleaved caspase-3 were upregulated, whereas Bcl-2 expression levels were downregulated in RSV-treated CRC cells compared with control cells. The results indicated that RSV might activate the mitochondrial apoptotic pathway by increasing ROS release. The present study suggested that RSV possessed antitumour activity against CRC by modulating an ROS-mediated mitochondrial apoptotic pathway.