Innovative Strategies in Oral Carcinoma: Disrupting Cell Signaling for Therapeutic Advances.

OBJECTIVE

This study aimed to evaluate the therapeutic efficacy of multi-pathway inhibition, targeting EGFR, MAPK, and PI3K/Akt in oral carcinoma.

METHODS

In vitro experiments were conducted using human oral carcinoma cell lines (HSC-3 and SCC-4) treated with EGFR, MAPK, and PI3K/Akt inhibitors individually and in combination. Cell viability was assessed using the MTT assay, apoptosis with Annexin V-FITC/PI staining, and pathway inhibition through Western blot. In vivo, nude mice (n=30, equal gender distribution) with xenograft tumours were treated with the same inhibitors, and tumour volume was measured over a period of 3 weeks.

RESULTS

Combination therapy reduced cell viability by 65% (vs. 40-45% for monotherapies) and increased apoptosis to 55% (vs. 25-30% for monotherapies). In vivo, tumour volume decreased by 64% with combination therapy (vs. 28-44% for monotherapies). Western blot analysis confirmed synergistic suppression of all three pathways in the combination group (p<0.05 for all comparisons).

CONCLUSION

Multi-pathway inhibition significantly enhances therapeutic efficacy in oral carcinoma by concurrently disrupting EGFR, MAPK, and PI3K/Akt signaling.