Farhan Mohd, Rizvi Asim, Ahmad Aamir, Aatif Mohammad, Alam Mir Waqas, Hadi Sheikh Mumtaz
Department of Basic Sciences, Preparatory Year Deanship, King Faisal University, Al-Ahsa 31982, Saudi Arabia.
Department of Kulliyat, Faculty of Unani Medicine, Aligarh Muslim University, Aligarh 202002, India.
Biomedicines. 2022 Mar 12;10(3):664. doi: 10.3390/biomedicines10030664.
The possible roles of elevated endogenous copper levels in malignant cells are becoming increasingly understood at a greater depth. Our laboratory has previously demonstrated that tea catechins have the ability to mobilize endogenous copper and undergo a Fenton-like reaction that can selectively damage cancer cells. In this communication, by using a diverse panel of malignant cell lines, we demonstrate that the ability of the catechin family [(-)-epigallocatechin-3-gallate (EGCG), (-)-epigallocatechin (EGC), (-)-epicatechin (EC), and (+)-catechin (C)] to induce apoptosis is dependent on their structure. We further confirm that reactive oxygen species (ROS) are the terminal effectors causing copper-mediated DNA damage. Our studies demonstrate the role of cellular copper transporters CTR1 and ATP7A in the survival dynamics of malignant cells post-EGCG exposure. The results, when considered together with our previous studies, highlight the critical role that copper dynamics and mobilization plays in cancer cells and paves the way for a better understanding of catechins as nutraceutical supplements for malignancies.
恶性细胞内源性铜水平升高的潜在作用正被更深入地理解。我们实验室先前已证明，茶儿茶素能够调动内源性铜并发生类似芬顿反应，从而可选择性地损伤癌细胞。在本通讯中，通过使用多种恶性细胞系，我们证明儿茶素家族[（-）-表没食子儿茶素-3-没食子酸酯（EGCG）、（-）-表没食子儿茶素（EGC）、（-）-表儿茶素（EC）和（+）-儿茶素（C）]诱导细胞凋亡的能力取决于其结构。我们进一步证实，活性氧（ROS）是导致铜介导的DNA损伤的终末效应因子。我们的研究证明了细胞铜转运蛋白CTR1和ATP7A在EGCG暴露后恶性细胞存活动态中的作用。这些结果与我们先前的研究一起，突出了铜动态和调动在癌细胞中所起的关键作用，并为更好地理解儿茶素作为恶性肿瘤营养补充剂铺平了道路。
