Role of c-Src in Carcinogenesis and Drug Resistance

Simple Summary The human body relies on essential proteins for cellular growth and development, which are synthesized according to the genetic code contained within the DNA (gene). However, if a gene malfunctions, abnormal proteins can result and lead to uncontrolled cell growth, ultimately contributing to the formation of cancerous tumors. The c-Src gene serves as a prime example of a dysregulated gene that results in the synthesis of abnormal protein that has been associated with the development of numerous types of cancer in humans. c-Src is a crucial player in the pathogenesis of cancer in both humans and other animals. It activates several proteins in cancer development, and aids established cancers in evading chemotherapeutic drugs through various mechanisms, facilitating drug resistance.Abstract The aberrant transformation of normal cells into cancer cells, known as carcinogenesis, is a complex process involving numerous genetic and molecular alterations in response to innate and environmental stimuli. The Src family kinases (SFK) are key components of signaling pathways implicated in carcinogenesis, with c-Src and its oncogenic counterpart v-Src often playing a significant role. The discovery of c-Src represents a compelling narrative highlighting groundbreaking discoveries and valuable insights into the molecular mechanisms underlying carcinogenesis. Upon oncogenic activation, c-Src activates multiple downstream signaling pathways, including the PI3K-AKT pathway, the Ras-MAPK pathway, the JAK-STAT3 pathway, and the FAK/Paxillin pathway, which are important for cell proliferation, survival, migration, invasion, metastasis, and drug resistance. In this review, we delve into the discovery of c-Src and v-Src, the structure of c-Src, and the molecular mechanisms that activate c-Src. We also focus on the various signaling pathways that c-Src employs to promote oncogenesis and resistance to chemotherapy drugs as well as molecularly targeted agents.