DNA methylationin normal and tumour virus-transformed cells in tissue culture I. The level of DNA methylation in BHK21 cells and in BHK21 cells transformed by polyoma virus (PyY cells)

Rubery, Eileen; Newton, Alison A.

doi:10.1016/0005-2787(73)90247-5

Cited by 34 publications

(10 citation statements)

References 21 publications

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“…The MeCyt content of DNA from BHK21 cells was 2.22%. This value was in fairly good agreement with that reported elsewhere (30). The MeCyt levels in the DNA from hamster cells transformed by Adl2 were significantly (about 40%) higher than in nontransformed BHK21 cells.…”

Section: Resultssupporting

confidence: 82%

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DNA methylation in adenovirus, adenovirus-transformed cells, and host cells.

Günthert¹,

Schweiger²,

Stupp³

et al. 1976

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

137

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DNAs of adenovirus type 2 and type 12 contain low amounts of methylated bases (0.01 and 0.02% N6-methyladenine per adenine, if any, and 0.04 and 0.06% 5-methylcytosine per cytosine for type 2 and type 12, respectively), whereas the DNA of the mammalian host cells contains much more 5-methylcytosine (3.57% for human KB cells). The Methylation of DNA was determined by a sensitive method based on two consecutive steps of two-dimensional thin-layer chromatography of the radioactively labeled DNA bases. By this procedure the detection limits of 5-methylcytosine and N6-methyladenine could be lowered to 0.01% per main base. During replication of adenoviruses in permissive human cells, a large amount of viral DNA is synthesized in the nucleus of the host cell (1-3). Viral DNA accounts for 30-50% of the total intracellular DNA at late times after infection (2, 3). Concomitantly with the onset of viral DNA replication, host DNA synthesis is drastically reduced (4).In previous DNA base analyses of mammalian cells 3-6% 5-methylcytosine (MeCyt) per cytosine (Cyt) was found (5, 6), while N6-methyladenine (MeAde) could not be detected (7,8).Little is known about the biological role of DNA methylation. There are reports on tissue specificities in the content of MeCyt in mammalian cells (5,6,9). Certain developmental stages are associated with variations in the content of methylated DNA bases in pro-and eukaryotes (10, 11). The only established function of certain DNA methyltransferases is the modification of DNA in bacteria leading to resistance against restriction endonucleases of the same specificity (12, 13).Since it is presumed that synthesis of adenovirus DNA in human cells is mediated, at least in part, by the host replication system, one would expect viral DNA to show the methylation pattern characteristic of host DNA. However, in contrast to host -DNA, adenovirus DNA has a low level of methylation. Comparison of untransformed cells and cells transformed by adenovirus has shown a difference in the levels of DNA methyl- (Calbiochem). The method of further purification has been described (21).In some experiments the total cellular DNA and the nonencapsidated viral DNA were isolated from Ad2-infected KB cells 40-48 hr after infection. Cell extracts were prepared by ultrasonic treatment, and the virions were isolated by equilibrium sedimentation in CsCl density gradients with a mean density of 1.334 g/cm3 as described (3). All free intracellular DNA was recovered from the pellet of this gradient and recentrifuged to equilibrium in a CsCl density gradient with a mean density of 1.70 g/cm3.Purification of Viral and Cellular DNA. The DNA was precipitated with two volumes of ethanol and kept for 4 hr at -20°. Traces of RNA were removed by hydrolysis in 0.25 M KOH 16-18 hr at 37°. Subsequently, the DNA was again pre-3923

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Section: Resultssupporting

confidence: 82%

“…In comparison to nontransformed hamster cells, elevated levels of MeCyt have been reported for cells transformed by polyoma virus (30) and Rous sarcoma virus (32 (11). However, T7 DNA accepts methyl groups in vitro (34).…”

Section: Resultsmentioning

confidence: 99%

DNA methylation in adenovirus, adenovirus-transformed cells, and host cells.

Günthert¹,

Schweiger²,

Stupp³

et al. 1976

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

137

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“…A recent statistical analysis of tumours occuring in patients over 50 years old suggested that the tumours studied, and their numbers, could be related to a decrease in the integrity of the genome (Dix et al, 1980 (Rubery & Newton, 1973;Browne & Burdon, 1977;Greene et al, 1975;DeWichter et al, 1971;Berneman et al, 1978). Groudine et al (1981) (Breznik & Cohen, 1982).…”

Section: -Mc Depletion During Tumour Developmentmentioning

confidence: 99%

5-Methylcytosine depletion during tumour development: An extension of the miscoding concept

Nyce¹,

Weinhouse²,

Magee³

1983

Br J Cancer

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Perhaps the most ubiquitous aspect of tumours and the neoplastic cells of which they are composed is their loss of the ability to control cellular functions in a normal way. During the development of the malignant state, the neoplastic cell becomes increasingly refractory to both the internal and external stimulae which integrate its normal counterparts into functional tissues and organ systems. This lack of integration is associated with alterations in the expression of a host of gene products, including, for example, the ectopic biosynthesis of hormones (

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“…BK, JC (possible carcinogens), and Merkel cell (causative agent) polyomavirus have been implicated in human cancers . To our knowledge, in 1973, first attempts performed to detect the correlation between viruses and host cell DNA methylation . Researchers sought the level of DNA methylation in normal BHK21 and polyomavirus‐transformed BHK21 cells.…”

Section: Polyomavirusesmentioning

confidence: 99%

DNA methyltransferases in virus‐associated cancers

Charostad

Astani

Goudarzi

et al. 2018

Reviews in Medical Virology

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Summary Human tumor viruses are either casually linked or contribute in the development of human cancers. Viruses can stimulate oncogenesis through affecting diverse biological pathways in human cells. Growing data have demonstrated frequent involvement of one of the most characteristic parts of cellular epigenetic machinery, DNA methylation, in the oncogenesis. DNA methylation of cellular genes is catalyzed by DNA methyltransferases (DNMTs) as a key effector enzyme in this process. Dysregulation of DNMTs can cause aberrant gene methylation in promoter of cancer‐related genes including tumor suppressor genes, resulting in gene silencing. In this regard, the role of tumor viruses is remarkable. Here, in this review, we used published information to elucidate whether tumor viruses are able to manipulate DNMT regulation, and if so, what are its consequences in the process of oncogenesis. This essay also aims to shed light on which cellular pathways have been engaged by viruses to induce DNMTs.

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DNA methylationin normal and tumour virus-transformed cells in tissue culture I. The level of DNA methylation in BHK21 cells and in BHK21 cells transformed by polyoma virus (PyY cells)

Cited by 34 publications

References 21 publications

DNA methylation in adenovirus, adenovirus-transformed cells, and host cells.

DNA methylation in adenovirus, adenovirus-transformed cells, and host cells.

5-Methylcytosine depletion during tumour development: An extension of the miscoding concept

DNA methyltransferases in virus‐associated cancers

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