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MCU-i4, a mitochondrial Ca2+ uniporter modulator, induces breast cancer BT474 cell death by enhancing glycolysis, ATP production and reactive oxygen species (ROS) burst

Year: 2024
Type: article
Abstract: Objectives: uptake, ATP production, and cancer cell proliferation. The objective of this study was to examine MCU inhibition as an anti-cancer mechanism. Methods: and potential, glycolytic rate, generation of ATP, and reactive oxygen species, were examined in breast cancer BT474 cells. Results: release via inositol 1,4,5-trisphosphate receptors (IP3R) and ryanodine receptors (RYR). Unexpectedly, MCU-i4 enhanced glycolysis and ATP production; it also triggered a large production of reactive oxygen species (ROS) and mitochondrial membrane potential collapse. Conclusion: Cytotoxic mechanisms of MCU-i4 in cancer cells involved enhanced glycolysis and heightened formation of ATP and ROS. It is conventionally believed that cancer cell death could be caused by inhibition of glycolysis. Our observations suggest cancer cell death could also be induced by increased glycolytic metabolism.
DOI: 10.32604/or.2024.052743
Authors: EDMUND CHEUNG SO, KAR-LOK WONG, LOUIS W. C. CHOW, CHIN-MIN CHUANG, CING YU CHEN, CHENG-HSUN WU, LIAN-RU SHIAO, YUK-MAN LEUNG, YI-PING HUANG, TING-TSZ OU
Institutions: China Medical University, An-Nan Hospital, Chang Jung Christian University, Kuang Tien General Hospital, Unimed Medical Institute, China Medical University Hospital, Providence University, Dayeh University
Language: English
Open Access status: hybrid
OpenAlex ID: W4401889650
FWCI: 0.923
Cites: 54
Cited by: 8
Related to: 10