Overexpression of the p53-inducible brain-specific angiogenesis inhibitor 1 [?] suppresses efficiently tumour angiogenesis.
Duda DG, Sunamura M, Lozonschi L, Yokoyama T, Yatsuoka T, Motoi F, Horii A, Tani K, Asano S, Nakamura Y, Matsuno S
First Department of Surgery, Tohoku University Medical School, 1-1 Seiryomachi, Aoba-ku, 980-8574 Sendai, Japan.
The brain-specific angiogenesis inhibitor 1 [?] gene has been isolated in an attempt to find fragments with p53 “functional” binding sites. As reported herein and by others, brain-specific angiogenesis inhibitor 1 [?] expression is present in some normal tissues, but is reduced or lost in tumour tissues. Such data and its particular structure prompted the hypothesis that brain-specific angiogenesis inhibitor 1 [?] may act as a mediator in the local angiogenesis balance. We herein demonstrate that brain-specific angiogenesis inhibitor 1 [?] over-expression suppresses tumour angiogenesis, delaying significantly the human tumour growth in immunodeficient mice. The inhibitory effect of brain-specific angiogenesis inhibitor 1 [?] was documented using our intravital microscopy system, strongly implicating brain-specific angiogenesis inhibitor 1 [?] as a mediator in the control of tumour angiogenesis. In contrast, in vitro tumour cell proliferation was not inhibited by brain-specific angiogenesis inhibitor 1 [?] transfection, whereas some level of cytotoxicity was assessed for endothelial cells. Immunohistochemical analysis of tumour samples confirmed a reduction in the microvessel density index in brain-specific angiogenesis inhibitor 1 [?]-overexpressing tumours. At messenger level, moderate changes could be detected, involving the down-regulation of vascular endothelial growth factor and collagenase-1 expression. Furthermore, brain-specific angiogenesis inhibitor 1 [?] expression that was lost in a selection of human cancer cell lines could be restored by wild-type p53 adenoviral transfection. Brain-specific angiogenesis inhibitor 1 [?] should be considered for gene therapy and development of efficient drugs based on endogenous antiangiogenic molecules.
Br. J. Cancer (2002)
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