Transformation of human epidermal cells by transfection with plasmid containing simian virus 40 DNA linked to a neomycin gene in a defined medium

The Immunohistochemical Characterisation of an SV40-immortalised Human Corneal Epithelial Cell Line

“…Carcinoma cell lines have often been reported to express CKs that are different from those of their cell type of origin (23,38,39). Primary cells may also produce other CKs, in addition to or as an alternative to the CKs of their tissue of origin (40)(41)(42)(43). The expression of the simple epitheliumspecific CKs 7, 8, 18 and 19 has been reported in the SV40-immortalised human keratinocyte cell lines originating from epidermis (44)(45)(46)(47).…”

Mammalian cell lines can be efficiently established in vitro upon expression of the SV40 large T antigen driven by a promoter sequence derived from the human vimentin gene

“…Even cells derived from tumors, in most cases, exhibit such a pattern of limited division and proliferation. The SV40 early genes have been introduced into a wide range of cells, and the induced phenotypes have been extensively studied ( [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20], human cells reviewed in [21,22]), showing that these cells may retain some of their initial characteristics of differentiated state, including responses to inducers: angiotensin-converting enzyme was occasionally detectable in transformed endothelial cells [6], Schwann cell lines synthesised specific proteins [16], major keratins in transformed epidermal cells were similar to those found in their normal counterparts [17], bronchial epithelial cells retained the ability to undergo squamous diffel'entiation when exposed to TPA or TGF-~ [15], transformed vascular smooth muscle cells had normal dose-* In memoriam to Daniel Sandoz ** Correspondence and reprints response curves to heparin [19], breast epithelial cell lines can differentiate along the myo-epithelial-like cell pathway [20], embryonal cells may still be induced to differentiate with retinoic acid [13]. The maintenance of the immortalized phenotype is dependent on the presence of the large T protein [2], involving gene activation of transcription factors, ie stimulating Ha-ras and trans-acting factor Spl at the mRNA level and affecting the transcription factor PEAl, and also involving protein-protein interaction with "anti-oncogene products" such as p53, pll0 Rb and p120, and with enhancer-binding proteins such as AP2 (reviewed in [3][4][5]).…”

“…The maintenance of the immortalized phenotype is dependent on the presence of the large T protein [2], involving gene activation of transcription factors, ie stimulating Ha-ras and trans-acting factor Spl at the mRNA level and affecting the transcription factor PEAl, and also involving protein-protein interaction with "anti-oncogene products" such as p53, pll0 Rb and p120, and with enhancer-binding proteins such as AP2 (reviewed in [3][4][5]). The SV40 early genes have been introduced into a wide range of cells, and the induced phenotypes have been extensively studied ( [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20], human cells reviewed in [21,22]), showing that these cells may retain some of their initial characteristics of differentiated state, including responses to inducers: angiotensin-converting enzyme was occasionally detectable in transformed endothelial cells [6], Schwann cell lines synthesised specific proteins [16], major keratins in transformed epidermal cells were similar to those found in their normal counterparts [17], bronchial epithelial cells retained the ability to undergo squamous diffel'entiation when exposed to TPA or TGF-~ [15], transformed vascular smooth muscle cells had normal dose-* In memoriam to Daniel Sandoz ** Correspondence and reprints response curves to heparin [19], breast epithelial cell lines can differentiate along the myo-epithelial-like cell pathway [20], embryonal cells may still be induced to differentiate with retinoic acid [13].…”