An increased high-mobility group A2 expression level is associated with malignant phenotype in pancreatic exocrine tissue

被引:93
作者
Abe, N
Watanabe, T
Suzuki, Y
Matsumoto, N
Masaki, T
Mori, T
Sugiyama, M
Chiappetta, G
Fusco, A
Atomi, Y
机构
[1] Kyorin Univ, Sch Med, Dept Surg 1, Tokyo 1818611, Japan
[2] Kyorin Univ, Sch Med, Dept Clin Pathol, Tokyo 1818611, Japan
[3] Inst Nazl Tumori Fdn Senatore Pascale, I-80131 Naples, Italy
[4] Univ Naples Federico II, CNR, Ctr Endocrinol & Oncol Sperimentale, Dipartimento Biol & Patol Cellulare & Mol, I-80131 Naples, Italy
关键词
HMGA2; pancreatic cancer; RT-PCR; immunostaining;
D O I
10.1038/sj.bjc.6601391
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The altered form of the high-mobility group A2 (HMGA2) gene is somehow related to the generation of human benign and malignant tumours of mesenchymal origin. However, only a few data on the expression of HMGA2 in malignant tumour originating from epithelial tissue are available. In this study, we examined the HMGA2 expression level in pancreatic carcinoma, and investigated whether alterations in the HMGA2 expression level are associated with a malignant phenotype in pancreatic tissue. High-mobility group A2 mRNA and protein expression was determined in eight surgically resected specimens of non-neoplastic tissue (six specimens of normal pancreatic tissue and two of chronic pancreatitis tissue) and 27 pancreatic carcinomas by highly sensitive reverse transcriptase-polymerase chain reaction (RT-PCR) techniques and immunohistochemical staining, respectively. Reverse transcriptase-polymerase chain reaction analysis revealed the expression of the HMGA2 gene in non-neoplastic pancreatic tissue, although its expression level was significantly lower than that in carcinoma. Immunohistochemical analysis indicated that the presence of the HMGA2 gene in non-neoplastic pancreatic tissue observed in RT-PCR reflects its abundant expression in islet cells, together with its focal expression in duct epithelial cells. Intense and multifocal or diffuse HMGA2 immunoreactivity was noted in all the pancreatic carcinoma examined. A strong correlation between HMGA2 overexpression and the diagnosis of carcinoma was statistically verified. Based on these findings, we propose that an increased expression level of the HMGA2 protein is closely associated with the malignant phenotype in the pancreatic exocrine system, and accordingly, HMGA2 could serve as a potential diagnostic molecular marker for distinguishing pancreatic malignant cells from non-neoplastic pancreatic exocrine cells.
引用
收藏
页码:2104 / 2109
页数:6
相关论文
共 37 条
[1]  
Abe N, 1999, CANCER RES, V59, P1169
[2]  
Abe N, 2000, CANCER RES, V60, P3117
[3]   Pancreatic endocrine function and glucose transporter (GLUT)-2 expression in rat acute pancreatitis [J].
Abe, N ;
Watanabe, T ;
Ozawa, S ;
Masaki, T ;
Mori, T ;
Sugiyama, M ;
Ishida, H ;
Nagamatsu, S ;
Atomi, Y .
PANCREAS, 2002, 25 (02) :149-153
[4]   Transgenic mice expressing a truncated form of the high mobility group I-C protein develop adiposity and an abnormally high prevalence of lipomas [J].
Arlotta, P ;
Tai, AKF ;
Manfioletti, G ;
Clifford, C ;
Jay, G ;
Ono, SJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (19) :14394-14400
[5]  
ASHAR HR, 1995, CELL, V82, P57
[6]   Increase in AP-1 activity is a general event in thyroid cell transformation in vitro and in vivo [J].
Battista, S ;
de Nigris, F ;
Fedele, M ;
Chiappetta, G ;
Scala, S ;
Vallone, D ;
Pierantoni, GM ;
Megar, T ;
Santoro, M ;
Viglietto, G ;
Verde, P ;
Fusco, A .
ONCOGENE, 1998, 17 (03) :377-385
[7]  
Battista S, 1999, CANCER RES, V59, P4793
[8]  
BERLINGIERI MT, 1995, MOL CELL BIOL, V15, P1545
[9]   Expression of collagenase (MMPZ), stromelysin (MMP3) and tissue inhibitor of the metalloproteinases (TIMP1) in pancreatic and ampullary disease [J].
Bramhall, SR ;
Stamp, GWH ;
Dunn, J ;
Lemoine, NR ;
Neoptolemos, JP .
BRITISH JOURNAL OF CANCER, 1996, 73 (08) :972-978
[10]   Truncated and chimeric HMGI-C genes induce neoplastic transformation of NIH3T3 murine fibroblasts [J].
Fedele, M ;
Berlingieri, MT ;
Scala, S ;
Chiariotti, L ;
Viglietto, G ;
Rippel, V ;
Bullerdiek, J ;
Santoro, M ;
Fusco, A .
ONCOGENE, 1998, 17 (04) :413-418