Dexmedetomidine Suppresses Mitochondrial Autophagy and Apoptosis While Promoting Proliferation in Breast Cancer Cells in vitro via PI3K/AKT Signaling.

[RESEARCH PURPOSE] To investigate how dexmedetomidine (DEX) controls the proliferation and death of breast cancer cells.

[METHODS] Human breast cancer cells were cultured in vitro with DEX at different concentrations (25, 50, 100 ng/mL) or 30 μM LY294002. Cancer cell viability, proliferation, apoptosis and the expression of Microtubule-associated protein light chain 3 (LC3)-II/LC3-I protein were separately analyzed using cell counting kit 8 (CCK-8), colony formation, flow cytometry and Western blot assays after DEX treatment. The effect of DEX on mitochondrial membrane potential (MMP) level in cancer cells was determined using immunofluorescence. The expressions of B cell lymphoma-2 (Bcl-2), Bcl-2 associated X (Bax), phosphatidylinositol 3-kinase (PI3K), phosphorylated (p)-PI3K, protein kinase B (AKT) and p-AKT in DEX-treated cancer cells were measured by Western blot.

[RESULTS] DEX promoted cell growth activity and proliferation, inhibited cell autophagy and apoptosis and down-regulated the ratio of LC3-II/LC3-I to reverse the effect of LY294002 on breast cancer cells. DEX also abrogated LY294002-induced down-regulation of MMP, p-PI3K/PI3K, p-AKT/AKT and Bcl-2 and up-regulation of Bax in breast cancer cells.

[CONCLUSION] DEX may promote the development of breast cancer cells while preventing cancer cell autophagy and apoptosis in vitro via PI3K/AKT signaling.