Abstract
The information for protein synthesis is given by the genes.These proteins are responsible for controlling functions like cell growth, differentiation, cell maturation, and cell death. In the case of genetic mutations, the protein functions get disturbed leading to a drastic shift in the normal physiological functions of cell growth, differentiation, and proliferation, making the normal cell cancerous. The Harvey rat sarcoma virus (HRAS) gene is an oncogene that belongs to the rat sarcoma virus (RAS) family. HRAS gene provides the instructions for making the HRAS protein that plays an important role in regulating cell division and when the HRAS gene gets mutated it gets involved in initiating cancer. HRAS mutation has been frequently noted in head and neck cancers; however, the mechanism of HRAS mutation involved in the initiation of oral squamous cell carcinoma (OSCC) still remains unexplored. An elaborate systematic literature search was done in PubMed, Scopus, and Web of Science databases. It was found that the Ras-dependent mutations affect the involved upstream and downstream components of the Ras-Raf-MAPK(rat sarcoma virus-rapidly accelerated fibrosarcoma-mitogen-activated protein kinase) pathway deregulating the signal leading to tumorigenesis. The Ras mutation can affect the Ras-Raf-MAPK pathway at different stages. The disease caused is based on the frequency of the HRAS mutation and it can lead to diverse cellular outcomes as it is mainly associated with cell division, differentiation, growth, survival, and the cell cycle. The crosstalk between the signaling pathways is controlled by the signaling molecules resulting in the creation of molecular networks. The balance of these molecular networks is very important to determine the cellular outcome. This systematic review inspects the molecular network of HRAS and its vital role in carcinogenesis. It is aimed at exploring and summarizing the contributions of the HRAS mutation involved in the pathogenesis of OSCC.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
