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

Chen,Yao‑Li; Chen,Po‑Ming; Ming,Ying‑Zi; Lin,Ping‑Yi; Chu,Chih‑Ping; Chu,Pei‑Yi

doi:10.3892/ol.2017.7137

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

Authors:
- Yao‑Li Chen
- Po‑Ming Chen
- Ying‑Zi Ming
- Ping‑Yi Lin
- Chih‑Ping Chu
- Pei‑Yi Chu
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Affiliations: School of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan, R.O.C., Research Assistant Center, Show Chwan Memorial Hospital, Changhua 50008, Taiwan, R.O.C., Transplantation Center, Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China, Department of General Surgery, Changhua Christian Hospital, Changhua 50008, Taiwan, R.O.C., Department of Pathology, Show Chwan Memorial Hospital, Changhua 50008, Taiwan, R.O.C.
Published online on: October 4, 2017 https://doi.org/10.3892/ol.2017.7137
Pages: 7461-7466

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Abstract

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.

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