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

Abstract

<h3>Background/Aim:</h3> 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. <h3>Materials and Methods:</h3> 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 <i>via</i> CompuSyn software. <h3>Results:</h3> 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 (CI&lt;1). The combination induced greater apoptosis and more pronounced G₂/M arrest compared with either agent alone, demonstrating a clear synergistic effect. <h3>Conclusion:</h3> BI-2536 in combination with β-glucan exhibits synergistic anticancer effects <i>in vitro</i>, suggesting a promising strategy for treating colon and gastric cancers.