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Human chromosome 11 suppresses the tumorigenicity of adenovirus transformed baby rat kidney cells: Involvement of the wilms' tumor 1 gene
Author(s) -
Menke A. L.,
Van Ham R. C. A.,
Sonneveld E.,
Shvarts A.,
Stanbridge E. J.,
Miyagawa K.,
Van Der Eb A. J.,
Jochemsen A. G.
Publication year - 1995
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910630115
Subject(s) - wilms' tumor , biology , chromosome , gene , microbiology and biotechnology , cancer research , adenoviridae , kidney , suppressor , karyotype , tumor suppressor gene , carcinogenesis , endocrinology , genetic enhancement , genetics
Human chromosome 11 was introduced into adenovirus‐transformed baby rat kidney (BRK) cells by microcell‐mediated chromosome transfer. The resulting microcell hybrids (MCHs) showed a reduced ability to form tumors upon s.c. injection into athymic mice. Further analysis, with the use of defined deletion chromosomes of lip, indicated that the presence of region 11 p 13‐p 12 is necessary for the suppression of tumorigenicity. In contrast, the presence of region lip 15–14.1 appeared to increase the rate of tumor growth. Expression studies on the human Wilms' tumor I (WTI) and the insulin‐like growth factor II (IGF‐II) genes, which lie in regions 11 p 13 and 11 p 15, respectively, suggested the involvement of both genes in determining the degree of suppression of tumorigenicity. Finally, stable expression of a murine WTI protein in the adenovirus‐transformed cells resulted in almost complete suppression of tumorigenicity, establishing the WTI protein as a tumor suppressor in this cell system.