The role of Aryl Hydrocarbon Receptor (AhR) signaling pathway in oral squamous cell carcinoma (OSCC): preliminary results.

Authors

Renee Lee, University of California, BerkeleyFollow
Cui Xu, University of the Pacific Arthur A. Dugoni School of DentistryFollow
Leticia Ferreira, University of the Pacific Arthur A. Dugoni School of DentistryFollow
Ana Carolina Morandini, University of the Pacific Arthur A. Dugoni School of DentistryFollow
Erivan Ramos-Junior, University of the Pacific, Arthur A. Dugoni School of DentistryFollow

Lead Author Affiliation

Department of Biomedical Sciences

Introduction/Context/Diagnosis

OBJECTIVES: A large number of experimental and clinical studies suggest that the origin of oral squamous cell carcinoma (OSCC) is linked to environmental carcinogenesis (tobacco, alcohol). Among these environmental factors, cigarette smoking is the most studied and has been associated with increased susceptibility to OSCC by activating signaling pathways responsible for cancer initiation and progression. Besides nicotine, cigarette smoke also contains aryl hydrocarbon receptor (AhR) agonists, such as dioxin and benzo(a)pyrene. Aberrant AhR expression and AhR pathway activation are involved in several types of cancer. However, the relationship between AhR pathway activation and oral cancer progression is still unclear.

Methods/Treatment Plan

METHODS: The AhR mRNA expression in human tumor biopsies was determined by analyzing data in two publicly deposited datasets (GSE54861 and GDS4562). Cell culture: Oral cancer DOK cells were stimulated with StemXVivo EMT Inducing Media Supplement during 3 or 5 days. AhR expression was accessed by western blot.

Results/Outcome

RESULTS: In the present study, we first compared the relative expression of AhR using two GEO datasets. AhR mRNA expression was significantly higher in tumor biopsies compared to normal tissues. Next, we used an in vitro model to induce epithelial-mesenchymal transition (EMT) in oral cancer DOK cells to check the AhR expression. The results showed that AhR was upregulated (day three by 5.99 fold increase; day five by 5.56 fold increase) in EMT-induced cells compared to non-induced cells.

Significance/Conclusions

CONCLUSION: The ultimate goal of this project is to clarify whether AhR expression could serve as a diagnostic and/or prognostic biomarker to OSCC.

Comments/Acknowledgements

This work was supported by Research Interdisciplinary Project Award 03-Activity 122 from the University of the Pacific Arthur A. Dugoni School of Dentistry

Location

2nd floor clinic and reception waiting areas

Format

Poster