ArticleCancer cell international2024
Proapoptotic role of CDK1 in overcoming paclitaxel resistance in ovarian cancer cells in response to combined treatment with paclitaxel and duloxetine.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Mechanisms of Paclitaxel Resistance: Recent Advances and Future Perspectives.International journal of molecular sciences · 2026Review
- DNA replication stress and translational repression converge to drive CDK1- and caspase-dependent apoptosis in Ewing sarcoma.Oncogene · 2026Article
- α-Viniferin Induces Intrinsic Apoptosis in Triple-Negative Breast Cancer Cells and Synergizes With SB203580 Independently of p38 Mitogen-Activated Protein Kinase.Journal of breast cancer · 2026Article
- Tyrosine hydroxylase as a therapeutic target: insights from adrenergic nerve and TNBC cell interactions.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Characterization of novel anoikis-related genes as prognostic biomarkers and key determinants of the immune microenvironment in esophageal cancer.Frontiers in immunology · 2025Article
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12 authors.
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Abstract
backgroundPaclitaxel resistance and recurrence are major obstacles in ovarian cancer, which is the leading cause of death among gynecologic cancers. During cancer cell progression, cyclin-dependent kinase 1 (CDK1) drives cells through the G2 phase and into mitosis. In this study, we demonstrated that CDK1 played a crucial role in switching paclitaxel-resistant ovarian cancer cells from mitotic arrest to apoptosis following combined treatment with paclitaxel and duloxetine, an antidepressant known as a serotonin-norepinephrine reuptake inhibitor (SNRI).
methodsCell viability was assessed by MTT assay. Apoptotic cell death and mitochondrial membrane potential (MMP) were detected by flow cytometry. Protein expression levels were explored using western blotting. Mitochondrial and cytosolic fractionation were performed to determine the mitochondrial localization of proteins. Immunofluorescence was used to detect protein expression levels and localization.
resultsCombined treatment with paclitaxel and duloxetine induced apoptotic cell death in paclitaxel-resistant ovarian cancer cells. We suggested that combined treatment of these drugs induced CDK1 activation and increased mitochondrial localization of activated CDK1, which caused phosphorylation of the antiapoptotic Bcl-2 and Bcl-xL proteins. Selective CDK1 inhibitors blocked Bcl-2 and Bcl-xL phosphorylation induced by paclitaxel and duloxetine, and strongly suppressed apoptotic cell death. Furthermore, we demonstrated that S6K is a potential upstream mediator of the proapoptotic activation of CDK1.
conclusionTaken together, switching CDK1 to a proapoptotic role through the combination of paclitaxel and duloxetine could overcome paclitaxel resistance in ovarian cancer cells, providing promising therapeutic strategies for treating paclitaxel-resistant ovarian cancer.
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