@article{Nithya_Sakthisekaran_2015, title={IN SILICO DOCKING STUDIES ON THE ANTI-CANCER EFFECT OF THYMOQUINONE ON INTERACTION WITH PTEN- A REGULATOR OF PI3K/ AKT PATHWAY}, volume={8}, url={https://journals.innovareacademics.in/index.php/ajpcr/article/view/2344}, abstractNote={<p>Objective: The statistics on cancer imposes the urge to extend new methods to control this deadly form of the disease. Phosphatase and tensin<br />homolog located on chromosome 10q23 (PTEN) is inactivated in a subset and AKT is frequently activated in cancer. The PTEN is the central negative<br />regulator of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling cascade that influences multiple cellular functions including cell growth, survival,<br />proliferation and migration in a context-dependent manner. Dysregulation of this signaling pathway contributes to different types of cancers. The<br />objective of the study is to explore the anti-cancer potential of thymoquinone (TQ) by analyzing the interaction between TQ with the target protein<br />PTEN.<br />Methods: The three dimensional structure of TQ is designed using in-silico methods, and the structure of PTEN is obtained from National Center for<br />Biotechnology Information against protein data bank. The query sequence from 8 to 353 amino acids was found to be 85% homologous to ID5R. For<br />the target protein PTEN with 403 residues, protein families analysis covered the important domains in PTEN.<br />Result: TQ showed the binding energy of −7.37 Kcal/mol against PTEN with three hydrogen bonds.<br />Conclusion: Present study suggests that TQ might inhibit abnormal cell proliferation occurring in cancer by modulating the activity of PTEN,<br />a negative regulator of PI3K/AKT pathway.<br />Keywords: Cancer, Thymoquinone, Phosphatase and tensin homolog located on chromosome 10q23, Docking and hydrogen bonds.</p><h1> </h1>}, number={1}, journal={Asian Journal of Pharmaceutical and Clinical Research}, author={Nithya, Gajendran and Sakthisekaran, Dhanapal}, year={2015}, month={Jan.}, pages={192–195} }