Abstract
With the incidence rate of oral carcinogenesis increasing in the Southeast-Asian countries, due to increase in the consumption of tobacco and betel quid as well as infection from human papillomavirus, specifically type 16, it becomes crucial to predict the transition of premalignant lesion to cancerous tissue at an initial stage in order to control the process of oncogenesis. DEPDC1B, downregulated in the presence of E2 protein, was recently found to be overexpressed in oral cancer, which can possibly be explained by the disruption of the E2 open reading frame upon the integration of viral genome into the host genome. DEPDC1B mediates its effect by directly interacting with Rac1 protein, which is known to regulate important cell signaling pathways. Therefore, DEPDC1B can be a potential biomarker as well as a therapeutic target for diagnosing and curing the disease. However, the lack of 3D model of the structure makes the utilization of DEPDC1B as a therapeutic target difficult. The present study focuses on the prediction of a suitable 3D model of the protein as well as the analysis of protein-protein interaction between DEPDC1B and Rac1 protein using PatchDock web server along with the identification of allosteric or regulatory sites of DEPDC1B.
Highlights
The association of cervical carcinomas with human papillomaviruses (HPVs), a group of small DNA viruses, was first recognized by Meisels et al [1, 2]
To have a better understanding, 3D model of DEPDC1B is predicted in the study predicted using Swiss model and visualized using PyMol (Figure 2), wherein it was observed that the protein consists of six α helices
In order to have a detailed understanding of its role in oral cancer, the present study focused on predicting the 3D model of the protein DEPDC1B by taking RhoGAP
Summary
The association of cervical carcinomas with human papillomaviruses (HPVs), a group of small DNA viruses, was first recognized by Meisels et al [1, 2]. E7 protein binds to a tumor suppressor protein, pRb, resulting in the activation of E2F (transcription factor) which further stimulates the expression of proteins critical for DNA replication [9, 10] This unprepared onset of S-phase results in the initiation of apoptosis via p53, which, will not be initiated in the case of HPV infected cells owing to p53 inactivation by the viral E6 protein [11]. HPV E2 being a repressor of viral oncogenic protein is termed as viral tumor suppressor, which, upon the integration of HPV 16/18 genome into the host genome results in the disruption of E1 and E2 open reading frames (ORF) followed by unregulated transcription of the oncogenic proteins, E6 and E7 This upregulated transcription results in the initiation of oral oncogenesis [15]
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