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Mechanistically, SLC25A39 overexpression maintains mitochondrial function, while its deficiency disrupts mitochondrial protein import and complex I activity, resulting in excessive ROS generation, loss of mitochondrial membrane potential, DNA damage, ATP depletion, and impaired electron transport, ultimately triggering apoptosis

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Furthermore, flow conditions that promote invasion of MDA-MB-231 aggregates in collagen gels trigger the upregulation of mesenchymal (Vimentin and Snail1) and epithelial (E-Cadherin and keratin-8) genes [237]

doi: 10.3390/ijms21010055 37 LinTYLanWHChiuYFFengCLChiuCHKuoCJet al