An Overview of the Mitogenic RAS Effectors and its Therapeutic Approaches

Nowadays, cancer is one of the major public health problems in the worldwide. Ras is an oncoprotein that is mainly active in types of human cancers. A mutation has been observed in  Ras gene among the more 90% of cancers including  pancreatic, lung, and colon cancers. Ras proteins (N-Ras, H-Ras, and K-Ras) act as molecular switches and are activated via GTP binding and signaling cascades to control cellular processes such as cell proliferation, differentiation, adhesion, apoptosis, migration, and division. Conversion of GTP to GDP (inactive state) is achieved through the internal GTPase activity of the Ras gene.

This review article has been performed by searching Cancer, Ras, Pancreatic, Lung, and Colon keywords in various data bases such as NCBI, PubMed, Scopus, Science Direct, and Google Scholar.

Mutation in the Ras results in loss of internal GTPase activity and permanently activates the protein. In this scenario, a continuous signaling is achieved by Ras  leading to cell-free growth, avoidance of cell death mechanisms, and resistance to treatment. RASSF family of effectors or Ras inhibitors are involved in many of these pathways. Thus, RASSF proteins may act as Ras death effectors. It′s inactivation may also progress the development of Ras-dependent tumors.
Discussion and

In general, RASSF proteins represent an interesting and contradictory part of Ras that  can be used as a useful tool for targeting a large set of Ras-derived tumors.