We investigated the association between c-Src and the progression of hepatocellular carcinoma (HCC) and its underlying mechanisms. The relationship between c-Src expression and the occurrence and development of HCC was explored using GEPIA and further confirmed by western blotting analysis and real-time quantitative PCR. CCK-8, flow cytometry, Transwell, and wound-healing assays were conducted to analyze the effects of c-Src on the growth, cell cycle, apoptosis, migration, and infiltration of HCC cells. Mouse models of transplanted xenogeneic human tumors were constructed to explore the effects of c-Src on HCC tumor growth. Compared with that in adjacent normal liver tissues, the expression level of c-Src in HCC tissues was significantly increased and was negatively correlated with patient survival. These findings are consistent with those in the GEPIA database. Downregulation of c-Src expression can inhibit the growth, infiltration, and migration of HCC cells. c-Src impeded the translocation of YAP from the nucleus to the cytoplasm and promoted Yes-associated protein transcriptional activity. In vivo experiments showed that c-Src inhibition suppressed tumor growth in mice. We found that c-Src can promote the growth and tumorigenesis of HCC cells by activating the Hippo signaling pathway.

我们研究了 c-Src 与肝细胞癌 (HCC) 进展之间的关联及其潜在机制。利用GEPIA探讨c-Src表达与HCC发生发展的关系，并通过蛋白质印迹分析和实时定量PCR进一步证实。通过CCK-8、流式细胞术、Transwell和伤口愈合实验来分析c-Src对HCC细胞的生长、细胞周期、凋亡、迁移和浸润的影响。构建移植异种人类肿瘤的小鼠模型，以探讨 c-Src 对 HCC 肿瘤生长的影响。与癌旁正常肝组织相比，HCC组织中c-Src的表达水平显着升高，且与患者生存率呈负相关。这些发现与 GEPIA 数据库中的结果一致。下调c-Src表达可以抑制HCC细胞的生长、浸润和迁移。 c-Src 阻止 YAP 从细胞核易位到细胞质，并促进 Yes 相关蛋白转录活性。体内实验表明，c-Src 抑制可抑制小鼠肿瘤的生长。我们发现c-Src可以通过激活Hippo信号通路促进HCC细胞的生长和肿瘤发生。