Pakistan Journal of Pharmaceutical Sciences

Abstract: Background: Paclitaxel is used in oral cancer treatment, but drug sensitivity remains a concern. CHFR has been implicated in tumor regulation, yet its role in modulating paclitaxel sensitivity in oral cancer requires further investigation. Objectives: This study aimed to evaluate the effect of CHFR on enhancing the drug sensitivity of paclitaxel in oral cancer cells. Methods: A rat oral tumor model was established, followed by paclitaxel intervention. Observations included tongue tissue morphology, immune function, cell cycle, apoptosis, and the expression levels of NF-?B and CHFR proteins and mRNAs. Results: The modeling success rate was 100%, with visible tongue masses and ulceration. CHFR protein expression increased in the CHFR mimic group. The high-dose paclitaxel group showed the highest immune indices, increased G0/G1 phase cell proportion, and significantly decreased tumor cell viability. The CHFR mimic group exhibited the smallest tumor volume, marked tumor cell death, and active proliferation. CHFR downregulated NF-?B expression; CHFR mRNA was higher, and NF-?B mRNA lower, compared to the high-dose paclitaxel and CHFR mimic groups. Conclusion: CHFR enhances paclitaxel sensitivity in oral cancer cells by downregulating NF-?B, effectively inhibiting tumor cell activity and suppressing tumor progression.