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Boric acid enhances the antitumor effects of paclitaxel by modulating apoptosis, autophagy-related protein expression, and proinflammatory cytokine expression in OVCAR-3 ovarian cancer cells

Jun 2026 · Turkish Journal of Medical Sciences · Vol 56, pp. 1332 - 1342 · 0 citations · 43 references
Medicine

TL;DR

Evidence is provided that boric acid enhances the antitumor efficacy of paclitaxel in drug-resistant ovarian cancer cells through coordinated modulation of cell cycle progression, apoptosis, autophagy-related protein expression, and inflammatory signaling.

Abstract

Background/aim Ovarian cancer is the eighth most prevalent malignancy among women globally and ranks third among gynecological cancers in terms of incidence. The limited efficacy of standard chemotherapy, primarily due to intrinsic drug resistance and high recurrence rates, highlights the urgent need for novel therapeutic strategies that are both effective and selectively cytotoxic. Materials and methods This study aimed to investigate the combined effects of boric acid (BA), a biologically active boron compound with emerging antitumor potential, and paclitaxel (PTX), a conventional chemotherapeutic agent, on cell viability, cell cycle progression, apoptosis, autophagy-related protein expression, and inflammatory signaling in the chemoresistant OVCAR-3 ovarian cancer cell line. OVCAR-3 cells were treated with increasing concentrations of BA over varying time periods. The half-maximal inhibitory concentrations (IC50) of both BA and PTX were determined using the MTT assay. Flow cytometry was employed to assess cell cycle distribution and apoptosis via Annexin V staining. Additionally, immunofluorescence staining was performed to evaluate the expression of autophagy-related proteins (Beclin-1, LC3, and p62) and proinflammatory cytokines (TNF-α, IL-6, and IL-1β). Results The combination of BA and PTX resulted in significant G0/G1 phase cell cycle arrest and a marked increase in apoptotic cell death and the expression of autophagy-related proteins, leading to reduced cell viability in OVCAR-3 cells. Furthermore, cotreatment significantly modulated the expression of proinflammatory cytokines, suggesting a potential immunomodulatory effect associated with the observed cytotoxicity. Conclusion The findings of this study provide evidence that boric acid enhances the antitumor efficacy of paclitaxel in drug-resistant ovarian cancer cells through coordinated modulation of cell cycle progression, apoptosis, autophagy-related protein expression, and inflammatory signaling. These findings support the potential of BA as a promising adjuvant for combination chemotherapy in ovarian cancer.

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