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.

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 (IC Results: The combination of BA and PTX resulted in significant G 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.