Upregulated INHBA expression is associated with poor survival in gastric cancer

被引:228
作者
Wang, Quan [1 ]
Wen, Yu-Gang [1 ]
Li, Da-Peng [1 ]
Xia, Jun [1 ]
Zhou, Chong-Zhi [1 ]
Yan, Dong-Wang [1 ]
Tang, Hua-Mei [2 ]
Peng, Zhi-Hai [1 ]
机构
[1] Shanghai Jiao Tong Univ, Coll Med, Dept Gen Surg, Shanghai Peoples Hosp 1, Shanghai 200080, Peoples R China
[2] Shanghai Jiao Tong Univ, Coll Med, Dept Pathol, Shanghai Peoples Hosp 1, Shanghai 200080, Peoples R China
关键词
Microarray; Gastric cancer; Marker; Enrichment; Prognosis; GROWTH-FACTOR-BETA; GENE-EXPRESSION; ACTIVIN RECEPTOR; CLUSTER-ANALYSIS; INHIBIN; IDENTIFICATION; PATHWAYS; PROTEINS;
D O I
10.1007/s12032-010-9766-y
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Expression microarrays are widely used for investigating the candidate molecular targets in human cancer. While genome-wide expression signatures screened by gene set enrichment analysis (GSEA) were not performed in Chinese gastric cancer (GC). To gain new molecular targets for GC, GSEA analysis was performed. In the present study, GSEA were used to pick out differentially expressed gene sets of our database. Total RNA of paired tissue samples (n = 48) and a tissue microarray containing 132 paired tissues were used to further validate expression levels of INHBA and its correction with clinicopathological factors. Upregulated INHBA expression in gastric cancer was screened and further confirmed by qPCR and immunostaining analysis. Increased INHBA expression was significantly correlated with the diameter of cancer and depth of tumor invasion. Patients with higher expression levels of INHBA had a shorter disease-free survival rate. It was effective to gain new molecular targets for GC by GSEA analysis. INHBA may be a poor survival indicator of GC.
引用
收藏
页码:77 / 83
页数:7
相关论文
共 32 条
[1]   Activin receptor signaling [J].
Abe, Y ;
Minegishi, T ;
Leung, PCK .
GROWTH FACTORS, 2004, 22 (02) :105-110
[2]   A systematic, genome-wide, phenotype-driven mutagenesis programme for gene function studies in the mouse [J].
Nolan, PM ;
Peters, J ;
Strivens, M ;
Rogers, D ;
Hagan, J ;
Spurr, N ;
Gray, IC ;
Vizor, L ;
Brooker, D ;
Whitehill, E ;
Washbourne, R ;
Hough, T ;
Greenaway, S ;
Hewitt, M ;
Liu, XH ;
McCormack, S ;
Pickford, K ;
Selley, R ;
Wells, C ;
Tymowska-Lalanne, Z ;
Roby, P ;
Glenister, P ;
Thornton, C ;
Thaung, C ;
Stevenson, JA ;
Arkell, R ;
Mburu, P ;
Hardisty, R ;
Kiernan, A ;
Erven, H ;
Steel, KP ;
Voegeling, S ;
Guenet, JL ;
Nickols, C ;
Sadri, R ;
Naase, M ;
Isaacs, A ;
Davies, K ;
Browne, M ;
Fisher, EMC ;
Martin, J ;
Rastan, S ;
Brown, SDM ;
Hunter, J .
NATURE GENETICS, 2000, 25 (04) :440-443
[3]   Activins are critical modulators of growth and survival [J].
Brown, CW ;
Li, LN ;
Houston-Hawkins, DE ;
Matzuk, MM .
MOLECULAR ENDOCRINOLOGY, 2003, 17 (12) :2404-2417
[4]  
BURGER HG, 1988, ENDOCRINOLOGY, V122, P1701
[5]   Genetic analysis of the mammalian transforming growth factor-β superfamily [J].
Chang, H ;
Brown, CW ;
Matzuk, MM .
ENDOCRINE REVIEWS, 2002, 23 (06) :787-823
[6]   Epidemiology of gastric cancer [J].
Crew, Katherine D. ;
Neugut, Alfred I. .
WORLD JOURNAL OF GASTROENTEROLOGY, 2006, 12 (03) :354-362
[7]   THE ISOLATION AND PHYSIOLOGY OF INHIBIN AND RELATED PROTEINS [J].
DEKRETSER, DM ;
ROBERTSON, DM .
BIOLOGY OF REPRODUCTION, 1989, 40 (01) :33-47
[8]   Cluster analysis and display of genome-wide expression patterns [J].
Eisen, MB ;
Spellman, PT ;
Brown, PO ;
Botstein, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (25) :14863-14868
[9]   Identification of a binding site on the type II activin receptor for activin and inhibin [J].
Gray, PC ;
Greenwald, J ;
Blount, AL ;
Kunitake, KS ;
Donaldson, CJ ;
Choe, S ;
Vale, W .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (05) :3206-3212
[10]   Genome-wide DNA copy number analysis in pancreatic cancer using high-density single nucleotide polymorphism arrays [J].
Harada, T. ;
Chelala, C. ;
Bhakta, V. ;
Chaplin, T. ;
Caulee, K. ;
Baril, P. ;
Young, B. D. ;
Lemoine, N. R. .
ONCOGENE, 2008, 27 (13) :1951-1960