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Sv40‐induced immortalization and ras ‐transformation of human bronchial epithelial cells
Author(s) -
Reedel Roger R.,
De Silva Ruwani,
Duncan Emma L.,
Rogan Eileen M.,
Whitaker Noel J.,
Zahra David G.,
Ke Yang,
McMenamin Mary G.,
Gerwin Brenda I.,
Harris Curtis C.
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.2910610210
Subject(s) - transfection , carcinogenesis , oncogene , immortalised cell line , cell culture , sv40 large t antigen , mutant , biology , cancer research , malignant transformation , transformation (genetics) , microbiology and biotechnology , gene , genetics , cell cycle
Non‐tumorigenic SV40‐immortalized human cells may be transformed to tumorigenicity by activated oncogenes, but the molecular genetics of this process are still poorly understood. We describe here 4 SV40‐transformed bronchial epithelial (BE) cell lines that became immortalized after a period of crisis, and then transfection of 6 BE lines or sub‐lines with an activated c‐Ha‐ ras (EJ‐ ras ) oncogene. pSV 2 neo‐transfected cells did not form any tumors in athymic nude mice. Even though each of the EJ‐ ras ‐transfected lines was shown to be expressing the mutant ras gene, only one cell line, BEAS‐2B, and 2 of its sub‐lines were tumorigenic after transfection. We conclude that immortalization is not sufficient for BE cells to be transformed by the EJ‐ ras oncogene. Thus there are at least 2 unknown genetic events in this in vitro model of carcinogenesis: escape from crisis (immortalization), and development of ability to cooperate with activated ras in tumorigenic transformation. We found no evidence that either immortalization or ability to complement ras is related to abnormalities of the SV40 T antigens, of p110 RB or of p 53. © 1995 Wiley‐Liss, Inc .