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Losses of 3p, 11p, and 13q in ej/ ras ‐ transformable simian virus 40‐immortalized human uroepithelial cells
Author(s) -
Kao Chinghai,
Wu ShiQi,
Bhatthacharya Manju,
Meisner Lorraine F.,
Reznikoff Catherine A.
Publication year - 1992
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.2870040210
Subject(s) - clone (java method) , biology , transfection , gene , virus , simian , microbiology and biotechnology , plasmid , mutant , transformation (genetics) , cell culture , chromosome , in vitro , mutation , virology , genetics
Five independent clones of Simian virus 40 (SV40)‐immortalized human uroepithelial cells (CK/SV‐HUC) were established after transfection of HUC cultures from the same tissue donor with plasmids encoding SV40 large T and small t antigen genes. Each CK/SV‐HUC clone contained a unique SV40 integration site, and all expressed similar levels of SV40 mRNA. All five clones were nontumorigenic, but clones 2, 4, and 5 tumorigenically transformed after transfection at P19 with mutant EJ/ ras and also spontaneously after 40 serial passages in vitro. In contrast, CK/SV‐HUC clones 1 and 3 did not transform when either approach was used. These differences in transformability among CK/SV‐HUC clones could not be predicted based on differences in SV40 gene expression nor on any in vitro growth property tested. In cytogenetic analyses, a transformable clone showed losses of three chromosome arms containing putative cancer suppressor gene regions, including 3p14→pter, 13q, and 11p, whereas the nontransformable clones showed none of these losses. Thus these data indicate that genetic losses on 3p, 11p, and 13q may contribute to tumorigenic transformation of SV40‐immortalized human uroepithelial cells.