Association of Vimentin overexpression and hepatocellular carcinoma metastasis

被引:200
作者
Hu, L
Lau, SH
Tzang, CH
Wen, JM
Wang, WS
Xie, D
Huang, MH
Wang, Y
Wu, MC
Huang, JF
Zeng, WF
Sham, JST
Yang, MS
Guan, XY
机构
[1] Univ Hong Kong, Dept Clin Oncol, Hong Kong, Hong Kong, Peoples R China
[2] City Univ Hong Kong, Dept Biol & Chem, Hong Kong, Hong Kong, Peoples R China
[3] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Pathol, Guangzhou, Peoples R China
[4] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Hepatobilliary Surg, Guangzhou, Peoples R China
[5] Second Mil Med Univ, Eastern Hepatobilliary Surg Hosp, Shanghai, Peoples R China
关键词
Vimentin; hepatocellular carcinoma; metastasis; microarray;
D O I
10.1038/sj.onc.1206483
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The poor prognosis of hepatocellular carcinoma (HCC) has been associated with recurrence and metastasis. Recently, we established a pair of HCC cell lines from a primary (H2-P) and its matched metastatic (H2-M) HCC tumors. A high density of cDNA microarray with 9184 human cDNA was used to identify the differentially expressed genes between H2-P and H2-M. Comparing with H2-P, eight upregulated and six downregulated genes were detected in H2-M. One interesting finding is the overexpression of Vimentin (VIM), a well-defined intermediate filament, which has been linked to a more aggressive status in various tumors. The correlation of overexpression of VIM and HCC metastasis was studied by immunohistochemistry using a tissue microarray with 200 primary HCCs and 60 pairs of primary and matched metastatic HCC samples. Tissue microarray demonstrated that the overexpression of VIM was significantly associated with HCC metastasis (P<0.01). This finding strongly suggests that the overexpression of VIM may play an important role in the metastasis of HCC.
引用
收藏
页码:298 / 302
页数:5
相关论文
共 25 条
[1]   Nonsurgical treatment of hepatocellular carcinoma [J].
Aguayo, A ;
Patt, YZ .
SEMINARS IN ONCOLOGY, 2001, 28 (05) :503-513
[2]  
Aldamassi M., 2001, PRACTICAL GUIDE MICR
[3]  
BENZEEV A, 1985, CANCER RES, V45, P2632
[4]   Definition of the tumor protein D52 (TPD52) gene family through cloning of D52 homologues in human (hD53) and mouse (mD52) [J].
Byrne, JA ;
Mattei, MG ;
Basset, P .
GENOMICS, 1996, 35 (03) :523-532
[5]   Recognition of polyadenylate RNA by the poly(A)-binding protein [J].
Deo, RC ;
Bonanno, JB ;
Sonenberg, N ;
Burley, SK .
CELL, 1999, 98 (06) :835-845
[6]   P53 PROTEIN AND VIMENTIN IN INVASIVE DUCTAL NOS BREAST-CARCINOMA - RELATIONSHIP WITH SURVIVAL AND SITES OF METASTASES [J].
DOMAGALA, W ;
STRIKER, G ;
SZADOWSKA, A ;
DUKOWICZ, A ;
HAREZGA, B ;
OSBORN, M .
EUROPEAN JOURNAL OF CANCER, 1994, 30A (10) :1527-1534
[7]  
FAN C, 1995, ONCOLOGY, V52, P498
[8]  
Gilles C, 1999, J CELL SCI, V112, P4615
[9]  
Gilles C, 1996, J PATHOL, V180, P175, DOI 10.1002/(SICI)1096-9896(199610)180:2<175::AID-PATH630>3.0.CO
[10]  
2-G