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. 2021 Sep 9;11:682710. doi: 10.3389/fonc.2021.682710

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Copyright © 2021 Wang, Gao, Hu, Zeng, Yang, Chen and Wang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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SLC25A21 overexpression induces cell apoptosis by the α-KG-mediated ROS pathway in BCa. (A) SLC25A21 promoted the efflux of α-KG from the mitochondria to the cytosol. (B) The levels of α-KG in the mitochondria affected succinate production. (C) The upregulation of SLC25A21 promoted ROS accumulation in BCa cells. (D) The upregulation of SLC25A21 decreased Δψm in both BCa cell lines. (E) Western blot assays showed that SLC25A21 induced cyto C transfer from the mitochondria to the cytosol and increased the activation of caspase-9 and caspase-3 in BCa cells. (F) Immunohistochemistry showed that SLC25A21 increased the activation of caspase-9 and caspase-3 in BCa xenograft tissues. (G) Schematic diagram showing the mechanism of action of SLC25A21 on cell apoptosis in BCa. The results were reproducible in three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001.