ArticleBiochemical genetics2026
Fisetin Modulates Chemoresistance-Associated miR-21, miR-181a, miR-203, miR-101 and miR-381 in Capecitabine-Resistant HT29 Colorectal Cancer Cells.
Article in Biochemical genetics, 2026. 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
Capecitabine is a key component of colorectal cancer (CRC) chemotherapy; however, acquired resistance markedly limits its efficacy. MicroRNAs (miRNAs) are central regulators of drug response, and the flavonoid fisetin has been reported to exert anti-tumor and chemosensitizing effects. Here, we investigated whether fisetin modulates the expression of chemoresistance-associated miRNAs in a capecitabine-resistant CRC cell model. Candidate miRNAs were prioritized from the publicly available dataset GSE30894 using differential expression analysis, which identified miR-21, miR-181a, miR-203, miR-101, and miR-381 as differentially expressed between sensitive and resistant colorectal cancer cells. These miRNAs were quantified by RT-qPCR in parental HT29 and capecitabine-resistant HT29 (CR/HT29) cells under basal conditions and after 24-h exposure to capecitabine (40 µM), fisetin (120 µM), or the combination. Nuclear morphology was assessed by DAPI staining. At baseline, CR/HT29 cells showed lower expression of miR-381, miR-21, miR-203, and miR-101 and a trend towards higher miR-181a compared with parental HT29 cells. Treatment with capecitabine, fisetin, or their combination differentially modulated these miRNAs in the two cell lines. In both parental and resistant cells, fisetin-containing regimens reduced miR-21, while in CR/HT29 cells, fisetin significantly decreased miR-181a expression compared with fisetin-treated parental cells. Fisetin and fisetin + capecitabine also altered miR-203 and miR-101 levels, with a more pronounced suppression in HT29 than in CR/HT29 cells. These changes were accompanied by marked morphological alterations in resistant cells. Fisetin modulates chemoresistance-associated miRNAs in colorectal cancer, particularly in capecitabine-resistant HT29 cells, suggesting a chemosensitizing adjuvant role and offering an in vitro basis for in vivo studies.
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