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Xiaoxiao LIAN, Tao HAN, Kunmeng CUI, Yan WANG, Yongfang LIU, Tian GUO, Ruixue YANG, Ya WANG. Inhibition of Breast Cancer by Ethanol Extract of Hedyotis diffusa through Mitochondrial Apoptosis Mediated by Cytochrome c/Caspase-9[J]. Journal of Kunming Medical University.
Citation: Xiaoxiao LIAN, Tao HAN, Kunmeng CUI, Yan WANG, Yongfang LIU, Tian GUO, Ruixue YANG, Ya WANG. Inhibition of Breast Cancer by Ethanol Extract of Hedyotis diffusa through Mitochondrial Apoptosis Mediated by Cytochrome c/Caspase-9[J]. Journal of Kunming Medical University.

Inhibition of Breast Cancer by Ethanol Extract of Hedyotis diffusa through Mitochondrial Apoptosis Mediated by Cytochrome c/Caspase-9

  • Received Date: 2024-01-20
  •   Objective  To investigate the effects and potential mechanisms of Hedyotis diffusa extract (HDE) on breast cancer cell proliferation, migration and mitochondrial damage through the cytochrome c (Cyt-c)/cysteine aspartate aminotransferase-9 (Caspase-9) pathway.   Methods  Cell Counting Kit-8 (CCK-8) was used to detect breast cancer cell viability in each group. MCF7 breast cancer cells were continuously cultured and divided into control group, HDE group, and Cyt-c overexpression group. Immunofluorescence staining was used to detect the protein levels of Cyt-c and Caspase-9 in MCF7 cells. 5-ethynyl-2'-deoxyuridine (EdU) kit was used to detect MCF7 cell proliferation ability. Scratch assay was used to detect MCF7 cell migration ability. Flow cytometry was used to detect mitochondrial membrane potential levels in MCF7 cells. Enzyme-linked immunosorbent assay (ELISA) kit was used to detect adenosine triphosphate (ATP) content in MCF7 cells.   Results  Compared with the control group, the cell viability of BT474, SKBr-3, ZR-75-30, MCF7 and MDA-MB-453 cells in the HDE group was decreased (P < 0.05). MCF7 breast cancer cells were selected for subsequent studies. Compared with the control group, the HDE group showed increased expression of Cyt-c and Caspase-9 in MCF7 cells (P < 0.05), decreased cell proliferation and migration ability (P < 0.05), reduced mitochondrial membrane potential, and decreased ATP content (P < 0.05). Compared with the control group, the Cyt-c overexpression group showed decreased cell proliferation and migration ability (P < 0.05), reduced mitochondrial membrane potential, and decreased ATP content (P < 0.05).   Conclusion  HDE may inhibit breast cancer cell, and promote mitochondrial damage by activating Cyt-c/Caspase-9 pathway.
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