Protein kinase B (Akt) plays a very significant role in various cancers including oral cancer. However, it has three isoforms (Akt1, Akt2, and Akt3) and they perform distinct functions and even play contrasting roles in different cancers. Therefore, it becomes essential to evaluate the isoform-specific role of Akt in oral cancer. In the present study, an attempt has been made to elucidate the isoform-specific role of Akt in oral cancer. The immunohistochemical analysis of oral cancer tissues showed an overexpression of Akt1 and 2 isoforms but not Akt3. Moreover, the dataset of “The Cancer Genome Atlas” for head and neck cancer has suggested the genetic alterations of Akt1 and 2 tend to be associated with the utmost poor clinical outcome in oral cancer. Further, treatment of oral cancer cells with tobacco and its components such as benzo(a)pyrene and nicotine caused increased mRNA levels of Akt1 and 2 isoforms and also enhanced the aggressiveness of oral cancer cells in terms of proliferation, and clonogenic and migration potential. Finally, silencing of Akt1 and 2 isoforms caused decreased cell survival and induced cell cycle arrest at the G2/M phase. Akt1/2 silencing also reduced tobacco-induced aggressiveness by decreasing the clonogenic and migration potential of oral cancer cells. Moreover, silencing of Akt1 and 2 isoforms was found to decrease the expression of proteins regulating cancer cell survival and proliferation such as cyclooxygenase-2, B-cell lymphoma 2 (Bcl-2), cyclin D1, and survivin. Thus, the important role of Akt1 and 2 isoforms have been elucidated in oral cancer with in-depth mechanistic analysis.
Background: Head and Neck Squamous Cell Carcinoma (HNSCC) is commonly associated with tobacco and alcohol consumption. The aim of this study is to find the association between the risk factors with HNSCC in a small tribal population of Mizoram, North-East India. Methods: Data were obtained through consented questionnaires and Logistic Regression was used to calculate the Odds Ratio (OR) between the parameters and HNSCC. Result: Significant association was observed for smoking and alcohol with an OR of 6.703 and 4.527, respectively. The OR was found to increase with increase in smoking and alcohol consumption. Majority of the patients consumed local made alcohol and smoked the local made cigarettes known as Zozial. Moreover, the First-Degree Family History of Cancer showed a significant OR of 1.921 (95% CI: 1.040-3.547). Conclusion: Regardless of the duration of smoking or alcohol consumption, Family History of Cancer might influence the risk of HNSCC. Further screening is essential to evaluate the potential role of germline mutational effect on development of HNSCC in the population.
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