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肝细胞癌中的KRT80通过上皮-间质转化和PI3K/AKT途径发挥致癌作用。

KRT80 in hepatocellular carcinoma plays oncogenic role via epithelial-mesenchymal transition and PI3K/AKT pathway.

作者信息

Hua Ruheng, Yan Xiyue, He Jun, Wu Nuwa, Yu Wangjianfei, Yu Pengfei, Qin Lei

机构信息

Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.

Department of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Nantong, China.

出版信息

IUBMB Life. 2025 Jan;77(1):e2925. doi: 10.1002/iub.2925. Epub 2024 Nov 21.

Abstract

Hepatocellular carcinoma (HCC), a globally prevalent form of cancer, is featured by aggressive growth and early metastasis. Elucidating the underlying mechanism and identifying the effective therapy are critical for advanced HCC patients. In the study, we detect that KRT80 was upregulated in HCC samples. HCC patients with higher KRT80 are associated with worse overall survival after surgery. Gain-of and loss-of function studies show that KRT80 enhanced HCC cells proliferation, migration, invasion, and angiogenesis, whereas its silencing abolishes the effects in vivo and in vitro. Mechanistic investigation shows that KRT80 may function as an independent prognostic risk factor and act as an oncogene by influencing EMT and modulating the PI3K/AKT signaling pathway. Together, these findings suggest that KRT80 may be a potential oncogene and a good indicator in predicting prognosis. Targeting KRT80 can offer new insights into the prevention and treatment of HCC.

摘要

肝细胞癌(HCC)是一种全球流行的癌症形式,其特征是生长迅速且早期转移。阐明其潜在机制并确定有效的治疗方法对晚期HCC患者至关重要。在本研究中,我们检测到KRT80在HCC样本中上调。KRT80水平较高的HCC患者术后总生存期较差。功能获得和功能丧失研究表明,KRT80增强了HCC细胞的增殖、迁移、侵袭和血管生成,而其沉默则消除了体内和体外的这些作用。机制研究表明,KRT80可能作为一个独立的预后风险因素,并通过影响上皮-间质转化(EMT)和调节PI3K/AKT信号通路发挥癌基因作用。总之,这些发现表明KRT80可能是一种潜在的癌基因,也是预测预后的良好指标。靶向KRT80可为HCC的预防和治疗提供新的见解。

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