Open AccessHuman papillomavirus type 16 cooperates with activated ras and fos oncogenes in the hormone-dependent transformation of primary mouse cells.
Author(s) -
Tim Crook,
Alan Storey,
Neil Almond,
Kit Osborn,
L. V. Crawford
Publication year - 1988
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.85.23.8820
Subject(s) - biology , heterologous , transfection , microbiology and biotechnology , cell culture , provirus , carcinogenesis , long terminal repeat , cancer research , virology , gene , gene expression , genetics , genome
The effect of human papillomavirus (HPV) and activated oncogenes on the growth and morphology of primary baby mouse kidney (BMK) cells has been studied. Early region DNA from HPV types 16, 18, 31, and 33, but not type 6, under the transcriptional control of a heterologous, retroviral promoter cooperated with EJ-ras to produce cell lines that gave rise to carcinomas in syngeneic immunocompetent animals. The same HPV constructs, when cotransfected with a plasmid containing sequences from the Finkel-Biskis-Jinkins murine sarcoma virus provirus (v-fos), produced cell lines that were tumorigenic in nude mice. None of the other activated oncogenes tested, including activated c-myc, displayed any activity with HPV in this cotransfection assay. When the heterologous promoter was replaced by the homologous HPV16 promoter, the transforming effect of HPV16 with either EJ-ras or v-fos required the presence of either glucocorticoid or progestogen. Cell lines derived from transfection of HPV16 with either EJ-ras or v-fos required the continued presence of hormones for proliferation.