Transformation of dog embryo kidney cells by human herpesviruses

Yelle, Jocelyn; Hamelin, Claude

doi:10.1016/0309-1651(86)90023-8

Cited by 3 publications

(2 citation statements)

References 12 publications

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“…Normal JLR cells were efficiently transformed by SV40 and HCMV as described in [26,27]. Colonies of densely packed cells, slowly overgrowing the culture, were observed after 6-8 weeks of incubation at 37°C (1-2 foci/ 105 infected cells).…”

Section: Properties Of Immortalized Cellsmentioning

confidence: 99%

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Low tumorigenicity of canine cells transformed by the human cytomegalovirus

Yelle¹,

Lussier²,

Pramatarova³

et al. 1990

Biology of the Cell

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Dog embryo kidney cells transformed by the human cytomegalovirus (HCMV) were obtained after non-permissive infection or transfection with viral DNA digested by restriction endonuclease EcoR I. The transformed cells, growing rapidly and showing an unlimited division potential, could use medium with only 2% serum for growth, contained nuclear virus antigens, and formed small colonies (less than 0.2 mm) in agarose. From 40 mice inoculated with transformed canine cells, only one eventually developed a tumor. Results indicate that dog cells are immortalized but not tumorigenically transformed by the human cytomegalovirus.

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Section: Properties Of Immortalized Cellsmentioning

confidence: 99%

“…A system based on the utilization of canine cells was recently developed in our laboratory to study the immortalizing properties of different DNA viruses [27]. Preliminary experiments showed the transformation of dog cells by HCMV [26,27]. Our purpose here was to examine the immortalization status of these cell lines.…”

Section: Introductionmentioning

confidence: 99%

Low tumorigenicity of canine cells transformed by the human cytomegalovirus

Yelle¹,

Lussier²,

Pramatarova³

et al. 1990

Biology of the Cell

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Human cytomegalovirus IE1 and IE2 proteins are mutagenic and mediate “hit-and-run” oncogenic transformation in cooperation with the adenovirus E1A proteins

Shen

Zhu²,

Shenk

1997

Proc. Natl. Acad. Sci. U.S.A.

162

109

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Some epidemiological studies have suggested a possible link between human cytomegalovirus (HCMV) infection and various malignancies, and HCMV has been shown to transform cultured cells. However, viral DNA is not detected in most transformants, and the mechanism by which HCMV might contribute to oncogenesis has remained obscure. Here we show that the HCMV immediate early 1 and 2 genes can cooperate with the adenovirus E1A gene to generate transformed foci of primary baby rat kidney cells. HCMV gene expression is transient and viral DNA is not present in clonal cell lines derived from the transformed foci. We find that the HCMV immediate early proteins are mutagenic, and we propose that HCMV has the potential to contribute to oncogenesis through a ''hit-and-run'' mechanism, by inducing mutations in cellular genes.Serological and molecular studies have suggested a possible association of human cytomegalovirus (HCMV) with the development of human malignancies, including cervical carcinoma, colon carcinoma, and prostate cancer (reviewed in refs. 1-5). A variety of laboratory observations demonstrate that HCMV has oncogenic potential, supporting the idea that HCMV might contribute to the induction of human tumors. HCMV has been shown to induce cervical neoplasia in mice (6), it can morphologically transform human (7,8) as well as other mammalian (9 -11) cells in culture, and HCMVtransformed cells can form tumors in experimental animals (6,8). In vitro assays have identified three regions on the HCMV genome with transforming activity (reviewed in ref. 5). However, if HCMV infection does contribute to tumor induction in humans, the mechanism underlying HCMV-induced oncogenesis is very likely different from that of DNA viruses that are known to play a role in human malignancies. Whereas specific viral genes are present and expressed in tumors induced by agents such as Epstein-Barr virus and the human papillomaviruses, no specific HCMV DNA sequence element is reliably present and often no viral DNA can be detected in cells transformed by HCMV (reviewed in refs. 4 and 12).We have previously reported (13) that the two most abundantly expressed immediate-early gene products of HCMV, IE1 and IE2 (reviewed in ref. 14), inhibit the induction of apoptosis by tumor necrosis factor ␣ (TNF-␣) or the adenovirus E1A oncoproteins. The fact that the IE1 and IE2 gene products are able to inhibit apoptosis raised the interesting possibility that they might cooperate with the adenovirus E1A oncoproteins to transform primary rodent cells, as do the adenovirus E1B 19-kDa (E1B) protein and the cellular Bcl-2 protein, each of which can block apoptosis (15,16). In this report, we show that the IE1 and IE2 gene products can, indeed, cooperate with E1A to transform primary baby rat kidney (BRK) cells. Unexpectedly, however, we find that expression of the IE1 and IE2 proteins is transient; HCMV proteins and DNA are not present in transformed cell lines derived from the foci. The IE1 and IE2 gene products are mutagenic, and we propose that...

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HSV-2 Transformation: A Multistep Process Mediated by Distinct Mutagenic DNA Sequences and Viral Genes Includes Activation of the Ras/MEK/MAPK Mitogenic Pathway

Aurelian¹,

Smith²

2001

Monographs in Virology

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Transformation of dog embryo kidney cells by human herpesviruses

Cited by 3 publications

References 12 publications

Low tumorigenicity of canine cells transformed by the human cytomegalovirus

Low tumorigenicity of canine cells transformed by the human cytomegalovirus

Human cytomegalovirus IE1 and IE2 proteins are mutagenic and mediate “hit-and-run” oncogenic transformation in cooperation with the adenovirus E1A proteins

HSV-2 Transformation: A Multistep Process Mediated by Distinct Mutagenic DNA Sequences and Viral Genes Includes Activation of the Ras/MEK/MAPK Mitogenic Pathway

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