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.
正常细胞异常转化为癌细胞的过程，即癌变，是一个复杂的生物学过程，涉及先天性和环境性刺激引发的众多遗传及分子改变。Src家族激酶（SFK）是参与癌变信号通路的关键组分，其中c-Src及其致癌对应物v-Src常发挥重要作用。c-Src的发现历程展现了突破性科学发现对揭示癌变分子机制的重要价值。在致癌激活状态下，c-Src通过激活PI3K-AKT通路、Ras-MAPK通路、JAK-STAT3通路及FAK/Paxillin通路等多条下游信号通路，在细胞增殖、存活、迁移、侵袭、转移及耐药性等过程中发挥关键作用。本综述系统阐述c-Src与v-Src的发现历程、c-Src蛋白结构及其激活的分子机制，重点探讨c-Src通过多种信号通路促进肿瘤发生发展，以及对化疗药物和分子靶向药物产生耐药性的作用机制。
肿瘤(癌症)患者之家