PDF(Pubmed)
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.
摘要：
正常细胞向癌细胞的异常转化，被称为致癌作用，是一个复杂的过程，涉及许多遗传和分子改变，以响应先天和环境刺激。Src家族激酶（SFK）是与癌发生有关的信号通路的关键组成部分，c-Src及其致癌对应物v-Src通常起着重要作用。c-Src的发现代表了令人信服的叙述，突出了开创性的发现和对致癌作用的分子机制的宝贵见解。在致癌激活后，c-Src激活多个下游信号通路，包括PI3K-AKT通路，Ras-MAPK通路,JAK-STAT3通路，和FAK/Paxillin途径，这对细胞增殖很重要，生存,迁移,入侵,转移,和抗药性。在这次审查中,我们深入研究了c-Src和v-Src的发现，c-Src的结构，以及激活c-Src的分子机制。我们还关注c-Src用于促进肿瘤发生和对化疗药物以及分子靶向药物的耐药性的各种信号通路。
