EFNA1 ligand and its receptor EphA2: potential biomarkers for hepatocellular carcinoma

被引:73
作者
Cui, Xiang-Dan [1 ]
Lee, Mi-Jin [1 ]
Yu, Goung-Ran [1 ]
Kim, In-Hee [1 ]
Yu, Hee-Chul [2 ]
Song, Eun-Young [3 ]
Kim, Dae-Ghon [1 ]
机构
[1] Chonbuk Natl Univ Med Sch & Hosp, Div Gastroenterol & Hepatol, Dept Internal Med, Inst Med Sci, Jeonju, Jeonbuk, South Korea
[2] Chonbuk Natl Univ Med Sch & Hosp, Dept Surg, Jeonju, Jeonbuk, South Korea
[3] Korea Res Inst Biosci & Biotechnol, Lab Cellular Signaling Modulator, Taejon, South Korea
关键词
EFNA1; EphA2; HCC; molecular marker; progression; TYROSINE KINASE; EXPRESSION; IDENTIFICATION; PROLIFERATION; EPHRIN-A1; SURVIVAL; MARKERS; GENE; ECK;
D O I
10.1002/ijc.24798
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Novel biomarkers are needed for early detection and progression evaluation of hepatocellular carcinoma (HCC). The purpose of this study was to identify useful biomolecular markers for HCC. The 26 genes that encode membrane or secretory proteins were identified from cDNA microarray data. We further examined the expression of EFNA1 and its receptor EphA2 and determined their biological implications during the development and progression of HCC. The EFNA1 mRNA was overexpressed in most HCCs as compared with its expression in corresponding nontumor tissues (36 out of 40 cases, 90%), but EphA2 expression was noted in only half of the HCC tissues (20 of 40 cases, 50%). In most of the hepatoma cell lines, the EFNA1 protein expression was positively associated with alpha-fetoprotien (AFP) expression but inversely associated with EphA2 expression. Furthermore, EFNA1 levels were detectable in the supernatant of the cultured hepatoma cells and in the serum of patients with HCC. In contrast, EphA2 expression was prominent in highly invasive hepatoma cells, and its overexpression was significantly correlated with decreased differentiation (r = 0.0248, p < 0.010) and poor survival (p = 0.0453) for HCC patients. EFNA1 and EphA2 may be useful serum markers for the detection of HCC development and progression, respectively.
引用
收藏
页码:940 / 949
页数:10
相关论文
共 37 条
[1]   Expression of EphA2 and ephrin A-1 in carcinoma of the urinary bladder [J].
Abraham, S ;
Knapp, DW ;
Cheng, L ;
Snyder, PW ;
Mittal, SK ;
Bangari, DS ;
Kinch, M ;
Wu, L ;
Dhariwal, J ;
Mohammed, SI .
CLINICAL CANCER RESEARCH, 2006, 12 (02) :353-360
[2]   Functions of cell surface heparan sulfate proteoglycans [J].
Bernfield, M ;
Götte, M ;
Park, PW ;
Reizes, O ;
Fitzgerald, ML ;
Lincecum, J ;
Zako, M .
ANNUAL REVIEW OF BIOCHEMISTRY, 1999, 68 :729-777
[3]   Soluble Eph A receptors inhibit tumor angiogenesis and progression in vivo [J].
Brantley, DM ;
Cheng, N ;
Thompson, EJ ;
Lin, Q ;
Brekken, RA ;
Thorpe, PE ;
Muraoka, RS ;
Cerretti, DP ;
Pozzi, A ;
Jackson, D ;
Lin, C ;
Chen, J .
ONCOGENE, 2002, 21 (46) :7011-7026
[4]   Clinical management of hepatocellular carcinoma.: Conclusions of the Barcelona-2000 EASL Conference [J].
Bruix, J ;
Sherman, M ;
Llovet, JM ;
Beaugrand, M ;
Lencioni, R ;
Burroughs, AK ;
Christensen, E ;
Pagliaro, L ;
Colombo, M ;
Rodés, J .
JOURNAL OF HEPATOLOGY, 2001, 35 (03) :421-430
[5]   Antiangiogenic and antitumor efficacy of EphA2 receptor antagonist [J].
Dobrzanski, P ;
Hunter, K ;
Jones-Bolin, S ;
Chang, H ;
Robinson, C ;
Pritchard, S ;
Zhao, H ;
Ruggeri, B .
CANCER RESEARCH, 2004, 64 (03) :910-919
[6]   Receptor tyrosine kinase EphA2 is regulated by p53-family proteins and induces apoptosis [J].
Dohn, M ;
Jiang, JY ;
Chen, XB .
ONCOGENE, 2001, 20 (45) :6503-6515
[7]   Trends in survival of patients with hepatocellular carcinoma between 1977 and 1996 in the United States [J].
El-Serag, HB ;
Mason, AC ;
Key, C .
HEPATOLOGY, 2001, 33 (01) :62-65
[8]  
Herrem CJ, 2005, CLIN CANCER RES, V11, P226
[9]   Ephrin-A1 expression contributes to the malignant characteristics of α- fetoprotein producing hepatocellular carcinoma [J].
Iida, H ;
Honda, M ;
Kawai, HF ;
Yamashita, T ;
Shirota, Y ;
Wang, BC ;
Miao, H ;
Kaneko, S .
GUT, 2005, 54 (06) :843-851
[10]   A novel mechanism for p53 to regulate its target gene ECK in signaling apoptosis [J].
Jin, Y. Jenny ;
Wang, Jianli ;
Qiao, Changhong ;
Hei, Tom K. ;
Brandt-Rauf, Paul W. ;
Yin, Yuxin .
MOLECULAR CANCER RESEARCH, 2006, 4 (10) :769-778