ArticleAmerican journal of translational research2024
Capecitabine regulates proliferation and apoptosis of ovarian cancer SKOV3 cells via the miR-29b-3p/MMP16 molecular axis.
Article in American journal of translational research, 2024. 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
objectiveTo investigate the molecular mechanism by which capecitabine regulates the proliferation and apoptosis of ovarian cancer SKOV3 cells through the miR-29b-3p/MMP16 axis.
methodsSKOV3 ovarian cancer cells were treated with capecitabine, miR-29b-3p mimics, miR-29b-3p inhibitor, and MMP16 siRNA. Cell proliferation was measured using the CCK-8 assay, and apoptosis was assessed by flow cytometry. Changes in miR-29b-3p and MMP16 mRNA levels were analyzed via qRT-PCR, while protein expression of MMP16, Ki67, Caspase-3, and Bcl-2 were evaluated by Western blot. Target genes of miR-29b-3p were predicted using bioinformatics tools, and their interaction was validated through a luciferase reporter assay. Transfection of SKOV3 cells with a miR-29b-3p inhibitor or pcDNA-MMP16 was followed by capecitabine treatment, with subsequent analysis of cell proliferation and apoptosis.
resultsCapecitabine treatment reduced the viability of SKOV3 cells and promoted apoptosis, accompanied by increased miR-29b-3p expression and decreased MMP16 expression. Transfection with miR-29b-3p mimics or MMP16 siRNA also inhibited cell viability and enhanced apoptosis. Western blot analysis showed an increase in Ki67 and Caspase-3 expression and a decrease in Bcl-2 expression. Conversely, inhibition of miR-29b-3p or overexpression of pcDNA-MMP16 counteracted the effects of capecitabine, reversing the reduction in proliferation and the increase in apoptosis. Western blotting confirmed decreased Ki67 and Caspase-3 levels and increased Bcl-2 expression in these conditions.
conclusionCapecitabine enhances miR-29b-3p expression, leading to the downregulation of MMP16, thereby inhibiting proliferation and promoting apoptosis in ovarian cancer cells.
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