CHFR enhances the drug sensitivity of paclitaxel in oral cancer cells.

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-κB 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-κB expression; CHFR mRNA was higher, and NF-κB mRNA lower, compared to the high-dose paclitaxel and CHFR mimic groups.

CONCLUSION

CHFR enhances paclitaxel sensitivity in oral cancer cells by downregulating NF-κB, effectively inhibiting tumor cell activity and suppressing tumor progression.