@article {1914,
	title = {An In Silico Study to Explore the Role of EGFR in Ovarian Cancer},
	journal = {Pharmacognosy Journal},
	volume = {14},
	year = {2022},
	month = {December 2022},
	pages = {817-821},
	type = {Research Article },
	chapter = {817},
	abstract = {<p class="rtejustify">EGFR is a tyrosine kinase receptor that has a role in the tumorigenesis of many types of solid tumors. Aberrantly phosphorylated or overexpressed EGFR is associated with cellular proliferation, prevention of apoptosis, activation of invasion and metastasis, and stimulation of tumor-induced neovascularization. EGFR{\textquoteright}s hyperactivity has been observed in ovarian cancer. Although conventional chemotherapy and surgery for advanced ovarian cancer have improved over the years, still there is a critical need for the development of molecular targeted therapies. The major challenge for this approach is the complete understanding of the protein structure of this mega receptor. In this study, we explored this receptor using <em>in silico</em> tools. The protein structure of the EGFR kinase domain (PDB ID: 1M17) and co-crystal containing EGFR and PTP1B kinase domain fragment (PDB ID: 3I7Z) were obtained from the RCSB Protein Data Bank. We performed protein-protein docking using BioLuminate. It was found in this study that the DADEYL segment of EGFR (position 988-993) which includes autophosphorylated tyrosine at position 992, is the segment that is responsible for the overexpression of this receptor in ovarian cancer. There are currently two main classes of clinically-approved drugs which downregulate EGFR activity; tyrosine kinase inhibitors (TKIs) and monoclonal antibodies (Mabs). However, treatment with both type of therapies has been met with shortcomings. Therefore, there is a need for further studies to explore the suitable ligands that can downregulate its activity.</p>
},
	keywords = {EGFR, In silico study, Protein-protein docking, Tyrosine kinases},
	doi = {10.5530/pj.2022.14.173},
	author = {Vikash Jakhmola and Tarun Parashar and Pallavi Ghildiyal and ANM Ansori and Rajeev Kumar Sharma and N. G. Raghavendra Rao and Kapil Kalra and Nishan Singh and Nidhi Nainwal and Rajeev Kumar Singh and M. P Singh and Vishwadeepak Kimothi and Alok Bhatt and Ashish Dimri and Ravi Kumar and Amit Semwal and Nur Sofiatul Aini and Maksim Rebezov}
}
