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

Document Type : Research Articles

Authors

1 Dentistry Department, Al-Rafidain University College, Baghdad, Iraq.

2 Faculty of Health and Life Sciences, INTI International University, Nilai, Negeri Sembilan, Malaysia.

3 Medical Laboratory Techniques Department, Al-Rafidain University College, Baghdad, Iraq.

4 Al-Kindi Teaching Hospital, Baghdad, Iraq.

5 Department of Food Sciences, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, Bangi, Selangor, Malaysia.

Abstract

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.

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Asian Pacific Journal of Cancer Prevention
Volume 27, Issue 1
January 2026
Pages 227-232

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History

  • Receive Date: 09 June 2025
  • Revise Date: 16 August 2025
  • Accept Date: 15 January 2026

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