Synergistic Anticancer Effects of the PLK1 Inhibitor BI-2536 and β-Glucan in Colon and Gastric Cancer Cells

Background/Aim: Colon and gastric cancers are among the most prevalent gastrointestinal malignancies, often exhibiting poor prognosis due to resistance and recurrence. Polo-like kinase 1 (PLK1), a key regulator of mitosis, is frequently overexpressed in these cancers. BI-2536, a selective PLK1 inhibitor, has shown promising anticancer activity. β-Glucan, a natural immunomodulator, has also demonstrated anticancer potential. This study aimed to evaluate the antiproliferative, apoptotic, and cell cycle effects of BI-2536 alone and in combination with β-glucan on HT-29 colon and AGS gastric cancer cell lines. Materials and Methods: Cell viability was assessed using the XTT assay. Apoptosis and cell cycle profiles were evaluated using flow cytometry. The combination index (CI) was calculated using the Chou–Talalay method via CompuSyn software. Results: BI-2536 significantly inhibited proliferation and induced G2/M arrest and apoptosis in both cell lines. β-Glucan showed moderate cytotoxicity and enhanced BI-2536’s effects. Synergistic antiproliferative activity was observed at lower drug concentrations, such as 2-16 nM BI-2536 combined with 31.25-250 μg/ml β-glucan (CI2/M arrest compared with either agent alone, demonstrating a clear synergistic effect. Conclusion: BI-2536 in combination with β-glucan exhibits synergistic anticancer effects in vitro, suggesting a promising strategy for treating colon and gastric cancers.