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Differential expression of HOX genes in neoplastic and non‐neoplastic human astrocytes
Author(s) -
AbdelFattah R,
Xiao A,
Bomgardner D,
Pease CS,
Lopes MBS,
Hussaini IM
Publication year - 2006
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1939
Subject(s) - hox gene , neoplastic transformation , biology , gene , neoplastic cell , homeotic gene , gene expression , pathology , cancer research , genetics , cell , carcinogenesis , medicine
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 glioblastoma 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 (II/III), and glioblastoma multiforme. The differential expression of HOX genes in normal and neoplastic astrocytes suggests a role for these genes in brain tumourigenesis. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.