ArticleCancer cell international2025
Epigenetic potentiation of 5-fluorouracil by HDAC inhibitor quisinostat enhances antitumor effects in colorectal cancer.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- Targeting the Epigenome in Colorectal Cancer.International journal of molecular sciences · 2026Review
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5 authors.
Funding
Abstract
backgroundHistone deacetylase (HDAC) inhibitors have emerged as promising epigenetic therapeutics in cancer treatment; however, their clinical efficacy in solid tumors remains limited. Quisinostat is a potent pan-HDAC inhibitor with demonstrated anticancer activity in various malignancies. This study evaluates the therapeutic potential of Quisinostat, in combination with 5-fluorouracil (5-FU), in colorectal cancer (CRC) cell lines.
methodsThe effects of Quisinostat and 5-FU, as monotherapies and in combination, were investigated in HCT-116 and HT-29 CRC cell lines. H3K27 acetylation levels were assessed by immunofluorescence to evaluate epigenetic modulation. Cell viability, IC50 shifts, and proliferation were measured using resazurin assays and Ki-67 staining. Apoptosis and mitochondrial membrane potential (ΔΨm) were analyzed via Hoechst 33342/PI dual staining and JC-1 assays. Migration and epithelial-mesenchymal transition (EMT) phenotypes were evaluated through wound healing assays and E-cadherin/N-cadherin immunostaining.
resultsQuisinostat significantly increased H3K27 acetylation and enhanced the cytotoxic effect of 5-FU by lowering its IC50 in both cell lines. The combination treatment markedly suppressed proliferation, as evidenced by reduced Ki-67 expression. Quisinostat in combination with 5-FU significantly enhanced ΔΨm loss and apoptotic cell death. Furthermore, the combination treatment inhibited cell migration and reversed the EMT phenotype by increasing E-cadherin and decreasing N-cadherin expression.
conclusionQuisinostat enhances the antitumor efficacy of 5-FU in CRC cells by promoting histone acetylation, augmenting cytotoxic and apoptotic responses, and reversing EMT-associated migratory phenotypes. These findings support the potential of Quisinostat as an effective adjunct to 5-FU-based chemotherapy in CRC.
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