Cytohesin-2 is overexpressed in human
lung cancer and it activates cytoplasmic
ErbB receptors. Inhibition of
cytohesin-2 by
SecinH3 reduces growth of EGFR-dependent
lung cancer xenografts and improves the treatment of primarily EGFR-TKI-resistant
lung cancers.
Cytohesin-2 promotes HepG2 proliferation through the IGF pathway, and
VEGF-dependent initiation of angiogenesis by regulation of
VEGFR-2 internalization in endothelial cells, vessel permeability and ultimately endothelial proliferation. The purpose of this study was to evaluate the effects of
cytohesin-2 in
hepatocellular carcinoma (HCC). In the current study, we collected 40 HCC tissues and detected
cytohesin-2 mRNA expression in the 40 HCC tissues by using quantitative real-time polymerase chain reaction (qRT-PCR), as well as its
protein expression by using immunohistochemistry and western blot analysis. We found that
cytohesin-2 was more highly expressed in HCC compared to adjacent non-tumorous liver tissues, and
cytohesin-2 expression was significantly increased in specimens with high α-
fetoprotein and vascular invasion. Both univariate and multivariate analyses indicated that there is an association between
cytohesin-2 expression and overall survival (OS) and disease-free survival (DFS). Moreover, stratified analysis showed that patients in
tumor-node-
metastasis (TNM) stage I with higher
cytohesin-2 levels had shorter OS and DFS than those with lower
cytohesin-2 levels. In conclusion,
cytohesin-2 may identify low-and high-risk individuals with HCC and may be a valuable
indicator for stratifying prognosis of TNM stage I patients.
Cytohesin-2 may serve as a novel prognostic
biomarker for HCC.