YAP1基因在肝细胞癌中调控PI3K/AKT信号通路及其对细胞功能的影响

YAP1 Gene Regulates the PI3K/AKT Signaling Pathway in Hepatocellular Carcinoma and Its Impact on Cellular Functions

摘要: 目的：研究YAP1基因能否影响肝细胞癌，是否通过PI3K/AKT信号转导通路影响细胞功能。方法：通过生物信息学，从公共数据库下载多种常见肿瘤的数据和相应的临床信息，通过提取数据，最后保留合适的样本信息，通过R语言进行对应分析并通过细胞实验验证相关可能。结果：肝细胞癌组正常组织与病理组织之间存在差异性，YAP1在肝细胞癌中与多个靶点及免疫细胞相关。高表达YAP1的肝细胞癌患者预后差，且与chlid分级及AFP值可能有关。YAP1的表达更多集中在肿瘤细胞中。敲低YAP1后肿瘤细胞的增殖及侵袭能力变弱，且AKT及p-AKT蛋白表达量变低。加入SC79可使PI3K/AKT通路恢复，但通路的恢复并不能改变细胞功能学的变化。结论：YAP1在肝细胞癌中高表达且高表达YAP1的肝细胞癌患者生存预后较差。敲低YAP1可以抑制肝癌细胞的增殖与侵袭能力。YAP1可能通过PI3K/AKT信号通路导致肝癌的发生与发展。

Abstract: Objective: To investigate whether the YAP1 gene influences hepatocellular carcinoma (HCC) and whether it affects cellular functions through the PI3K/AKT signaling pathway. Methods: Bioinformatics analysis was conducted using data and clinical information from public tumor databases. Following data extraction, relevant samples were analyzed with R and validated through cell experiments. Results: Differences were observed between normal and pathological tissues in the HCC group. YAP1 was associated with multiple targets and immune cells in HCC. Patients with high YAP1 expression had a poor prognosis, potentially linked to Child-Pugh grade and AFP levels. YAP1 expression was predominantly concentrated in tumor cells. Knocking down YAP1 reduced the proliferation and invasion abilities of tumor cells, along with decreased expression of AKT and p-AKT proteins. Although SC79 restored the PI3K/AKT pathway, this restoration did not reverse the changes in cellular functions. Conclusion: YAP1 is highly expressed in HCC, and high YAP1 expression correlates with poor survival prognosis in HCC patients. Knocking down YAP1 inhibits the proliferation and invasion capabilities of HCC cells. YAP1 may contribute to the occurrence and progression of HCC through the PI3K/AKT signaling pathway.