Differential expression of HOX genes in neoplastic and non-neoplastic human astrocytes

被引:58
作者
Abdel-Fattah, R
Xiao, A
Bomgardner, D
Pease, CS
Lopes, MBS
Hussaini, IM
机构
[1] Univ Virginia, Dept Pathol, Sch Med, Charlottesville, VA 22908 USA
[2] UVA, Sch Med, Dept Cell Biol, Charlottesville, VA USA
关键词
HOX; astrocytes; glioblastoma; expression;
D O I
10.1002/path.1939
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
HOX genes are a large family of regulatory genes implicated in the control of developmental processes. HOX genes are involved in malignant transformation and progression of different types of tumour. Despite intensive efforts to delineate the expression profiles of HOX genes in other cell types, nothing is known regarding the global expression profile of these genes in normal human astrocytes and astrocytomas. The present study has analysed the expression profile of the 39 class I HOX genes in normal human astrocytes (NHA and E6/E7), two well-established ghoblastoma cell lines (U-87 MG and U-1242-MG), as well as neoplastic (WHO grades II/III and IV) and non-neoplastic temporal lobe specimens with hippocampal sclerosis and medically intractable epilepsy. RT-PCR, quantitative real-time PCR, immunocytochemistry, and western blot analyses revealed differential expression of nine HOX genes (A6, A7, A9, A13, B13, D4, D9, D10, and D13) in normal human astrocytic cell lines and non-neoplastic temporal lobe specimens. The data show that HOX genes are differentially expressed in neoplastic and non-neoplastic astrocytes and that multiple HOX genes are overexpressed in glioblastoma cell lines, astrocytomas and glioblastoma multiforme. The differential expression of HOX genes in normal and neoplastic astrocytes suggests a role for these genes in brain tumourigenesis. Copyright (c) 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
引用
收藏
页码:15 / 24
页数:10
相关论文
共 35 条
[1]  
AKAM M, 1987, DEVELOPMENT, V101, P1
[2]   HOXC5 and HOXC8 expression are selectively turned on in human cervical cancer cells compared to normal keratinocytes [J].
Alami, Y ;
Castronovo, V ;
Belotti, D ;
Flagiello, D ;
Clausse, N .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 257 (03) :738-745
[3]   Phorbol 12-myristate 13-acetate induces epidermal growth factor receptor transactivation via protein kinase Cδ/c-Src pathways in glioblastoma cells [J].
Amos, S ;
Martin, PM ;
Polar, GA ;
Parsons, SJ ;
Hussaini, IM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (09) :7729-7738
[4]   Classification of glioblastoma multiforme in adults by molecular genetics [J].
Benjamin, R ;
Capparella, J ;
Brown, A .
CANCER JOURNAL, 2003, 9 (02) :82-90
[5]  
Bodey B, 2000, ANTICANCER RES, V20, P1769
[6]   The translocation t(8;l6)(p11, p13) of acute myeloid leukaemia fuses a putative acetyltransferase to the CREB binding protein [J].
Borrow, J ;
Stanton, VP ;
Andresen, JM ;
Becher, R ;
Behm, FG ;
Chaganti, RSK ;
Civin, CI ;
Disteche, C ;
Dube, I ;
Frischauf, AM ;
Horsman, D ;
Mitelman, F ;
Volinia, S ;
Watmore, AE ;
Housman, DE .
NATURE GENETICS, 1996, 14 (01) :33-41
[7]   Overexpression of HOXA10 perturbs human lymphomyelopoiesis in vitro and in vivo [J].
Buske, C ;
Feuring-Buske, M ;
Antonchuk, J ;
Rosten, P ;
Hogge, DE ;
Eaves, CJ ;
Humphries, RK .
BLOOD, 2001, 97 (08) :2286-2292
[8]   Altered HOX and WNT7A expression in human lung cancer [J].
Calvo, R ;
West, J ;
Franklin, W ;
Erickson, P ;
Bemis, L ;
Li, E ;
Helfrich, B ;
Bunn, P ;
Roche, J ;
Brambilla, E ;
Rosell, R ;
Gemmill, RM ;
Drabkin, HA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (23) :12776-12781
[9]   In vivo expression of the whole HOX gene network in human breast cancer [J].
Cantile, M ;
Pettinato, G ;
Procino, A ;
Feliciello, I ;
Cindolo, L ;
Cillo, C .
EUROPEAN JOURNAL OF CANCER, 2003, 39 (02) :257-264
[10]   Hyperexpression of locus C genes in the HOX network is strongly associated in vivo with human bladder transitional cell carcinomas [J].
Cantile, M ;
Cindolo, L ;
Napodano, G ;
Altieri, V ;
Cillo, C .
ONCOGENE, 2003, 22 (41) :6462-6468