FOXD1-mTOR Signaling Pathway on Oral Squamous Cell Carcinoma and Its Inhibition by Rosemary Extract (Invitro-Study)

Document Type : Research Articles


1 Oral and Maxillofacial Pathology, Faculty of Dentistry, October 6 University, Cairo, Egypt.

2 Medical Biochemistry and Molecular Biology, Faculty of Medicine-Cairo University, Cairo, Egypt.

3 Medical Biochemistry and Molecular Biology, Faculty of Medicine- Badr University, Cairo, Egypt.

4 Department of Lab Technology, Faculty of Applied Medical Science, Misr University for Science andTechnology, Egypt.

5 Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Cairo University, Giza, Egypt.


Background: FOXD1 expression in oral squamous cell carcinoma remains uncovered. The aim was to detect the anticancer effect of Rosemary Extract RE through the evaluation of FOXD1 gene expression in (OSCC) by quantitative PCR. Methods: OSCC cell line was served as a control group. Moreover, the OSCC cell line (SCC-15) was treated with RE (OSCC/ RE group) at 24, 48, and 72 hs time intervals. We assessed the antioxidant activity of RE by evaluation of lipid peroxidation (MDA) and superoxide dismutase (SOD) levels. The cytotoxic effects of RE were examined by MTT assay. mTOR and LC3 I/II autophagy protein markers were assessed by western blot. Apoptosis activity was assessed. Results: The study results were statistically assessed. Intergroup comparisons were analyzed, whereas intragroup comparisons were conducted utilizing one-way repeated measures ANOVA, followed by multiple pairwise paired t-tests with Bonferroni correction revealed a significant increase of FOXD1 gene expression in the control OSCC group in comparison to the OSCC/RE group (p-value <0.001). A significant decrease of mTOR/LC3I/II proteins expression in the OSCC/RE group compared to the control OSCC group (p-value <0.001). Conclusion: FOXD1 can be considred a diagnostic biomarker for OSCC. RE inhibits autophagy of oral human cancer cells via mTOR/LC3I/II-dependent pathways and decrease caspase -3 apoptotic level.