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已发表论文
右美托咪定通过 PI3K/AKT 信号通路抑制体外培养的乳腺癌细胞的线粒体自噬和凋亡，同时促进其增殖
Authors Gu M, Xia Y, Qian J, Shao C, Li Y, Lu X, Qin X
Received 27 May 2025
Accepted for publication 21 November 2025
Published 20 December 2025 Volume 2025:17 Pages 1265—1278
DOI https://doi.org/10.2147/BCTT.S543090
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Pranela Rameshwar
Mengting Gu,* Yanfei Xia,* Jiang Qian, Caiqun Shao, Yujia Li, Xing Lu, Xiarong Qin
Anesthesiology Department, Zhejiang Hospital, Hangzhou, Zhejiang, 310013, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xiarong Qin, Anesthesiology Department, Zhejiang Hospital, No. 12 Lingyin Road, Xihu District, Hangzhou, Zhejiang, 310013, People’s Republic of China, Tel +571-87987373, Email qinxiarong111@126.com
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.
Keywords: dexmedetomidine, breast cancer, mitochondrial autophagy, apoptosis, PI3K/AKT signaling
Anesthesiology Department, Zhejiang Hospital, Hangzhou, Zhejiang, 310013, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xiarong Qin, Anesthesiology Department, Zhejiang Hospital, No. 12 Lingyin Road, Xihu District, Hangzhou, Zhejiang, 310013, People’s Republic of China, Tel +571-87987373, Email qinxiarong111@126.com
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.
Keywords: dexmedetomidine, breast cancer, mitochondrial autophagy, apoptosis, PI3K/AKT signaling