Human BCAS3 Expression in Embryonic Stem Cells and Vascular Precursors Suggests a Role in Human Embryogenesis and Tumor Angiogenesis

被引:27
作者
Siva, Kavitha [1 ]
Venu, Parvathy [1 ]
Mahadevan, Anita [2 ]
Shankar, S. K. [2 ]
Inamdar, Maneesha S. [1 ]
机构
[1] Indian Inst Sci, Jawaharlal Nehru Ctr Adv Sci Res, Mol Biol & Genet Unit, Bangalore 560012, Karnataka, India
[2] Natl Inst Mental Hlth & Neurosci, Dept Neuropathol, Bangalore 560029, Karnataka, India
关键词
D O I
10.1371/journal.pone.0001202
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Cancer is often associated with multiple and progressive genetic alterations in genes that are important for normal development. BCAS3 (Breast Cancer Amplified Sequence 3) is a gene of unknown function on human chromosome 17q23, a region associated with breakpoints of several neoplasms. The normal expression pattern of BCAS3 has not been studied, though it is implicated in breast cancer progression. Rudhira, a murine WD40 domain protein that is 98% identical to BCAS3 is expressed in embryonic stem (ES) cells, erythropoiesis and angiogenesis. This suggests that BCAS3 expression also may not be restricted to mammary tissue and may have important roles in other normal as well as malignant tissues. We show that BCAS3 is also expressed in human ES cells and during their differentiation into blood vascular precursors. We find that BCAS3 is aberrantly expressed in malignant human brain lesions. In glioblastoma, hemangiopericytoma and brain abscess we note high levels of BCAS3 expression in tumor cells and some blood vessels. BCAS3 may be associated with multiple cancerous and rapidly proliferating cells and hence the expression, function and regulation of this gene merits further investigation. We suggest that BCAS3 is mis-expressed in brain tumors and could serve as a human ES cell and tumor marker.
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共 34 条
[1]  
[Anonymous], COMPLEXITY
[2]   The breakpoint region of the most common isochromosome, i(17q), in human neoplasia is characterized by a complex genomic architecture with large, palindromic, low-copy repeats [J].
Barbouti, A ;
Stankiewicz, P ;
Nusbaum, C ;
Cuomo, C ;
Cook, A ;
Höglund, M ;
Johansson, B ;
Hagemeijer, A ;
Park, SS ;
Mitelman, F ;
Lupski, JR ;
Fioretos, T .
AMERICAN JOURNAL OF HUMAN GENETICS, 2004, 74 (01) :1-10
[3]  
Bärlund M, 2000, CANCER RES, V60, P5340
[4]   Characterization of the vasculogenic block in the absence of vascular endothelial growth factor-A [J].
Bautch, VL ;
Redick, SD ;
Scalia, A ;
Harmaty, M ;
Carmeliet, P ;
Rapoport, R .
BLOOD, 2000, 95 (06) :1979-1987
[5]  
Bergwerff M, 1998, CIRC RES, V82, P221
[6]  
Brinkschmidt C, 1997, J PATHOL, V181, P394
[7]   Angiogenesis in health and disease [J].
Carmeliet, P .
NATURE MEDICINE, 2003, 9 (06) :653-660
[8]  
Courjal F, 1997, CANCER RES, V57, P4368
[9]  
Cowan CA, 2004, NEW ENGL J MED, V350, P1353, DOI 10.1056/NEJMsr040330
[10]   CHARACTERIZATION OF ICAM-2 AND EVIDENCE FOR A 3RD COUNTER-RECEPTOR FOR LFA-1 [J].
DEFOUGEROLLES, AR ;
STACKER, SA ;
SCHWARTING, R ;
SPRINGER, TA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 174 (01) :253-267