ArticleMedical oncology (Northwood, London, England)2025
Sericin induces apoptosis in the ovarian cancer cell line (OVCAR-3) through the miR-34a-related pathway.
Article in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Human ovarian cancer is a highly aggressive malignancy in women, characterized by high mortality and poor prognosis. Dysregulation of microRNAs (miRNAs) plays a critical role in the pathogenesis of various cancers, including ovarian cancer. Among these, miR-34a functions as a tumor suppressor miRNA and represents a promising target for cancer therapy. Downregulation of miR-34a in ovarian cancer has been associated with disease initiation and progression. Sericin, a silk-derived glycoprotein, possesses diverse biological activities, including antioxidant, anti-inflammatory, and anticancer properties. The present study, for the first time, investigated the potential effects of sericin on miR-34a-mediated apoptotic pathways in the human ovarian cancer cell line OVCAR3. OVCAR3 cells were treated with sericin at concentrations of 2 mg/mL and 64 mg/mL for 48 h. The expression level of miR-34a was quantified using real-time quantitative PCR (qPCR), while the protein expression levels of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and the pro-apoptotic protein Bcl-2-associated X protein (BAX) were evaluated by Western blot analysis. Sericin treatment at both 2 mg/mL and 64 mg/mL significantly upregulated miR-34a expression and increased BAX protein levels in OVCAR3 cells. Moreover, sericin at 64 mg/mL markedly decreased Bcl-2 protein expression. Given the central role of Bcl-2 in conferring resistance to anticancer therapies and the importance of apoptosis dysregulation in tumor progression and therapeutic resistance, these findings suggest sericin as a promising anticancer agent. In summary, the results indicate that sericin exerts its anticancer effect, at least in part, through activation of a miR-34a-dependent apoptotic pathway.
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