BACKGROUND AND OBJECTIVES: Using the technique of differential hybridization of Atlas Human cDNA expression arrays, we previously reported the isolation of a G protein coupled receptor, CXCR-4, which is overexpressed in glioblastoma multiforme tumor tissue (GMTT) compared to normal brain tissue (NBT). METHODS: Using gene specific reverse transcriptase-polymerase chain reaction (RT-PCR) and in situ hybridization, we studied its expression in a variety of brain and breast tumor tissue samples. To demonstrate the requirement of CXCR-4 in glioblastoma cell proliferation an antisense construct was overexpressed. Glioblastoma cells were also treated with antibodies against CXCR-4 and its ligand, SDFbeta-1. RESULTS: Expression analysis indicated that CXCR-4 is overexpressed in 57% of the primary glioblastoma tissues and in 88% of the glioblastoma cell lines analyzed. Overexpression of CXCR-4 in glioblastoma cell lines enhanced their soft agar colony-forming capability. Expression of anti-sense CXCR-4 in glioblastoma cell lines caused neurite outgrowth and cellular differentiation. Treatment of glioblastoma cell lines with CXCR-4 and SDFbeta-1 specific antibodies caused inhibition of glioblastoma cell proliferation. CONCLUSIONS: On the basis of these results, we conclude that CXCR-4 gene is required for the proliferation of human glioblastoma tumors.
BACKGROUND AND OBJECTIVES: Using the technique of differential hybridization of Atlas Human cDNA expression arrays, we previously reported the isolation of a G protein coupled receptor, CXCR-4, which is overexpressed in glioblastoma multiforme tumor tissue (GMTT) compared to normal brain tissue (NBT). METHODS: Using gene specific reverse transcriptase-polymerase chain reaction (RT-PCR) and in situ hybridization, we studied its expression in a variety of brain and breast tumor tissue samples. To demonstrate the requirement of CXCR-4 in glioblastoma cell proliferation an antisense construct was overexpressed. Glioblastoma cells were also treated with antibodies against CXCR-4 and its ligand, SDFbeta-1. RESULTS: Expression analysis indicated that CXCR-4 is overexpressed in 57% of the primary glioblastoma tissues and in 88% of the glioblastoma cell lines analyzed. Overexpression of CXCR-4 in glioblastoma cell lines enhanced their soft agar colony-forming capability. Expression of anti-sense CXCR-4 in glioblastoma cell lines caused neurite outgrowth and cellular differentiation. Treatment of glioblastoma cell lines with CXCR-4 and SDFbeta-1 specific antibodies caused inhibition of glioblastoma cell proliferation. CONCLUSIONS: On the basis of these results, we conclude that CXCR-4 gene is required for the proliferation of humanglioblastoma tumors.
Authors: T Ponomaryov; A Peled; I Petit; R S Taichman; L Habler; J Sandbank; F Arenzana-Seisdedos; A Magerus; A Caruz; N Fujii; A Nagler; M Lahav; M Szyper-Kravitz; D Zipori; T Lapidot Journal: J Clin Invest Date: 2000-12 Impact factor: 14.808
Authors: Joshua B Rubin; Andrew L Kung; Robyn S Klein; Jennifer A Chan; YanPing Sun; Karl Schmidt; Mark W Kieran; Andrew D Luster; Rosalind A Segal Journal: Proc Natl Acad Sci U S A Date: 2003-10-31 Impact factor: 11.205
Authors: Moneeb Ehtesham; Elliot Min; Neil M Issar; Rebecca A Kasl; Imad S Khan; Reid C Thompson Journal: J Neurooncol Date: 2013-03-14 Impact factor: 4.130
Authors: Erica L Johnson; Rajesh Singh; Shailesh Singh; Crystal M Johnson-Holiday; William E Grizzle; Edward E Partridge; James W Lillard Journal: World J Surg Oncol Date: 2010-07-22 Impact factor: 2.754