Cigarette Smoke Effects on Oral Cancer

Objectives: Cigarette smoke (CS) can induce cellular damage via alterations in the 18 kDa translocator protein (TSPO) functions, leading to the development of lethal diseases such as oral cancer. Moreover, CS causes alterations in mitochondrial membrane potential (Δψ_M), reactive oxygen species generation, as well as other intracellular alteration resulting in cellular damage and cancer development.

• Understand the mechanism of the damaging effects of CS at the cellular level and on cancer development
• Examination of the protective role of our compounds against the effects of CS.

Methods:

• Various parameters were considered to investigate the contribution of smoking to oral cancer development.
• In vitro model was exposed to CS and further analysis performed of intracellular alterations, which can result in tissue damage and cancer development.
• Cells were pre-treated with TSPO compounds prior to exposure to CS, and their protective ability was examined

Results:

• Laboratory studies expressed significant time-dependent increase in cell death levels including both apoptosis and necrosis, ROS generation, and other mitochondrial processes.
• TSPO expression increased by 24% (p > 0.05) following 30 mins of CS exposure, and significantly increased by 43% (p < 0.05) and by 47% (p < 0.01) after 60 mins and 120 mins of CS exposure, respectively.
• Protective capability of our TSPO ligands was demonstrated against cell death, mitochondrial membrane potential collapse, ATP levels alterations, as well as other intracellular functions which result in cancer development.

Conclusion: CS is a major risk factor for oro-pharyngeal cancer development. The relation between CS and the various intracellular function is essential for understanding the mechanism through which CS inserts its deleterious effects, as well as the applicability of our patented compounds, developed in our laboratory, for protection against CS.