ArticleBreast cancer (Dove Medical Press)2025
Dexmedetomidine Suppresses Mitochondrial Autophagy and Apoptosis While Promoting Proliferation in Breast Cancer Cells in vitro via PI3K/AKT Signaling.
Article in Breast cancer (Dove Medical Press), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- The impact of using dexmedetomidine during surgery on the postoperative survival of cancer patients: a meta-analysis and systematic review of real-world studies.Frontiers in pharmacology · 2026Pooled it
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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