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Apoptin causes apoptosis in HepG‐2 cells via Ca2+ imbalance and activation of the mitochondrial apoptotic pathway.
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- Author(s): Yu, Xiaoyang; Wang, Tongxing; Li, Yue; Li, Yiquan; Bai, Bing; Fang, Jinbo; Han, Jicheng; Li, Shanzhi; Xiu, Zhiru; Liu, Zirui; Yang, Xia; Li, Yaru; Zhu, Guangze; Jin, Ningyi; Shang, Chao; Li, Xiao; Zhu, Yilong
- Source:
Cancer Medicine; Apr2023, Vol. 12 Issue 7, p8306-8318, 13p- Subject Terms:
- Source:
- Additional Information
- Abstract: Background: Apoptin is derived from the chicken anemia virus and exhibits specific cytotoxic effects against tumor cells. Herein, we found that Apoptin induced a strong and lasting endoplasmic reticulum (ER) stress response, Ca2+ imbalance, and triggered the mitochondrial apoptotic pathway. The aim of this study was to explore the mechanisms by which Apoptin exhibited anti‐tumor effects in HepG‐2 cells. Methods: The intracellular levels of calcium (Ca2+) were induced by ER stress and determined by electron microscopy, flow cytometry, and fluorescence staining. The mitochondrial injury was determined by mitochondrial membrane potential and electron microscopy. Western blotting was used to investigate the levels of key proteins in ER stress and the apoptotic pathway in mitochondria. The relationship between Ca2+ levels and apoptosis in Apoptin‐treated cells was analyzed using a Ca2+ chelator (BAPTA‐AM), flow cytometry, and fluorescence staining. We also investigated the in vivo effects of Ca2+ imbalance on the mitochondrial apoptotic pathway using tumor tissues xenografted on nude mice. Results: This study showed that Apoptin induced a strong and long‐ lasting ER stress and injury, which subsequently led to an imbalance of cellular Ca2+ levels, a reduction in the mitochondrial membrane potential, a significant extent image in the mitochondrial structure, and an increase in the expression levels of Smac/Diablo and Cyto‐C. Conclusions: In summary, Apoptin induced apoptosis in HepG‐2 cells via Ca2+ imbalance and activation of the mitochondrial apoptotic pathway. This study provided a new direction for antitumor research in Apoptin. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Cancer Medicine is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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