Phosphorylated AKT expression in tumor-adjacent normal tissue is associated with poor prognosis in patients with hepatocellular carcinoma

The AKT pathway serves important roles in tumor cell growth. Its overexpression is associated with poor prognosis in a number of types of cancer; however, the role of AKT in the role of the pathogenesis of hepatocellular carcinoma (HCC) remains unclear. The present study was undertaken to explore th...

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Bibliographic Details
Published in:Oncology letters 2017-12, Vol.14 (6), p.7461-7466
Main Authors: Chen, Yao-Li, Chen, Po-Ming, Ming, Ying-Zi, Lin, Ping-Yi, Chu, Chih-Ping, Chu, Pei-Yi
Format: Article
Language:English
Subjects:
Care and treatment
Development and progression
Gene expression
Genetic aspects
Health aspects
Hepatocellular carcinoma
Liver cancer
Medical prognosis
normal tissue
Oncogenes
Oncology
phosphorylated AKT
Phosphorylation
poor prognosis
Tumors
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Summary:The AKT pathway serves important roles in tumor cell growth. Its overexpression is associated with poor prognosis in a number of types of cancer; however, the role of AKT in the role of the pathogenesis of hepatocellular carcinoma (HCC) remains unclear. The present study was undertaken to explore the clinical relevance of phosphorylated AKT (p-AKT) in HCC. The level of p-AKT in tumor (TU) and paired adjacent normal liver (AN) tissue from 202 HCC patients was evaluated with immunohistochemistry. The results demonstrated that p-AKT was more highly expressed in TU than in AN tissue. Kaplan-Meier curves and Cox regression revealed that patients with a high expression of p-AKT (AN) exhibited reduced overall and relapse-free survival times; this was not observed at a statistically significant level in p-AKT (TU). Additionally, the high expression of p-AKT (AN) was positively correlated with hepatitis C virus (HCV) infection in HCC patients. These results support the hypothesis that AKT activation is a mechanism of HCV-induced hepatocarcinogenesis, suggesting that AKT can be a therapeutic target for the treatment of recurrent HCC subsequent to surgical resection.
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2017.7137