I am interested in investigating the role of sirtuins in oral cancer carcinogenesis. Oral cancer is the eighth most common cancer worldwide, and oral squamous cell carcinoma (OSCC) accounts for more than 90 % of all oral malignancies. The 5-year survival rate is approximately 50 %, which have not changed for decades. This underscores the need for new therapeutic targets to treat oral cancer. Sirtuins (SIRT1-7), an evolutionarily conserved family of NAD-dependant deacetylases, are the mammalian homologs of Sir2 gene, Silencing information regulator 2, which were first discovered in yeast.  This family is involved in a diverse of cellular responses and functions including gene silencing, development, cell survival, aging, and longevity.  This new area of research has been extensively studied and developed only within the last few years. There is an emerging role of this family in carcinogenesis, however; their role in oral cancer has not yet been investigated. 

       Our Studies show that specifically SIRT3 is overexpressed in oral squamous cell carcinoma (OSCC) in vitro and in vivo, compared to other sirtuins. Downregulation of SIRT3 inhibited OSCC cell growth and proliferation, and increased its sensitivity to radiation and cisplatin treatments. Our findings reveal a novel role for SIRT3 in oral cancer carcinogenesis as a modulator of cell proliferation and survival. This implicates SIRT3 as a new potential therapeutic target to treat oral cancer.

       In Summary, these studies will help us to better understand the signaling pathways and mechanisms whereby sirtuins can influence carcinogenesis in general, and oral cancer in particular. Thus, this may lead to the development of new potential therapeutic targets and approaches that may have a better chance of solving the problem of cellular cytotoxicity upon using conventional treatments, recurrence, and drug-induced resistance. Thus, hopefully improving the survival rate of oral cancer patients.