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DNA Methyltransferase Is a Downstream Effector of Cellular Transformation Triggered by Simian Virus 40 Large T Antigen
Open accessAbstract
This paper tests the hypothesis that DNA methyltransferase plays a causal role in cellular transformation induced by SV40 T antigen. We show that T antigen expression results in elevation of DNA methyltransferase (MeTase) mRNA, DNA MeTase protein levels, and global genomic DNA methylation. A T antigen mutant that has lost the ability to bind pRb does not induce DNA MeTase. This up-regulation of DNA MeTase by T antigen occurs mainly at the posttranscriptional level by altering mRNA stability. Inhibition of DNA MeTase by antisense oligonucleotide inhibitors results in inhibition of induction of cellular transformation by T antigen as determined by a transient transfection and soft agar assay. These results suggest that elevation of DNA MeTase is an essential component of the oncogenic program induced by T antigen.
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“Expression levels of DNMTs positively correlate to DNMT activity and thus to any global methylation trends observed (Slack et al., 1999).”
From The Epigenetics of Anxiety Pathophysiology: A DNA Methylation and Histone Modification Focused Review (2023) · cites this paper as Slack et al., 1999
Citations
Cites
Tumorigenic conversion of primary embryo fibroblasts requires at least two cooperating oncogenes
Land, H., Parada, L. F., & Weinberg, R. A. (1983) · Nature · doi:10.1038/304596a0 · Cited by 2,804
Research works printed but not linked: 33
- Razin, 1980, Science, 210, 604, 10.1126/science.6254144 · DOI
- Razin, 1984, Biochim. Biophys. Acta, 782, 331, 10.1016/0167-4781(84)90043-5 · DOI
- Adams, 1979, Biochim. Biophys. Acta, 561, 345, 10.1016/0005-2787(79)90143-6 · DOI
- Kautiainen, 1986, J. Biol. Chem., 261, 1594, 10.1016/S0021-9258(17)35981-1 · DOI
- Belinsky, 1996, Proc. Natl. Acad. Sci. U. S. A., 93, 4045, 10.1073/pnas.93.9.4045 · DOI
- Merlo, 1995, Nat. Med., 1, 686, 10.1038/nm0795-686 · DOI
- Nelkin, 1991, Blood, 77, 2431, 10.1182/blood.V77.11.2431.2431 · DOI
- Lee, 1996, Proc. Natl. Acad. Sci. U. S. A., 93, 10366, 10.1073/pnas.93.19.10366 · DOI
- Szyf, 1994, Trends Pharmacol. Sci., 7, 233, 10.1016/0165-6147(94)90317-4 · DOI
- MacLeod, 1995, J. Biol. Chem., 270, 11327, 10.1074/jbc.270.19.11327 · DOI
- Rouleau, 1995, J. Biol. Chem., 270, 1595, 10.1074/jbc.270.4.1595 · DOI
- Szyf, 1996, Pharmacol. Ther., 70, 1, 10.1016/0163-7258(96)00002-2 · DOI
- MacLeod, 1995, J. Biol. Chem., 270, 8037, 10.1074/jbc.270.14.8037 · DOI
- Ramchandani, 1997, Proc. Natl. Acad. Sci. U. S. A., 94, 684, 10.1073/pnas.94.2.684 · DOI
- Laird, 1995, Cell, 81, 197, 10.1016/0092-8674(95)90329-1 · DOI
- Brinster, 1984, Cell, 37, 367, 10.1016/0092-8674(84)90367-2 · DOI
- Tevethia, 1984, Virology, 137, 414, 10.1016/0042-6822(84)90234-4 · DOI
- Aaronson, 1968, Virology, 36, 254, 10.1016/0042-6822(68)90142-6 · DOI
- De Caprio, 1988, Cell, 54, 275, 10.1016/0092-8674(88)90559-4 · DOI · Paper page
- Levine, 1977, Virology, 77, 419
- Chuang, 1997, Science, 277, 1996, 10.1126/science.277.5334.1996 · DOI
- Almazan, 1992, Brain Res., 579, 234, 10.1016/0006-8993(92)90056-F · DOI
- Freedman, 1974, Cell, 3, 355, 10.1016/0092-8674(74)90050-6 · DOI
- Rouleau, 1992, J. Biol. Chem., 267, 7368, 10.1016/S0021-9258(18)42526-4 · DOI
- Szyf, 1991, J. Biol. Chem., 266, 10027, 10.1016/S0021-9258(18)99179-9 · DOI
- Clark, 1994, Nucleic Acids Res., 22, 2990, 10.1093/nar/22.15.2990 · DOI
- Vertino, 1996, Mol. Cell. Biol., 16, 4555, 10.1128/MCB.16.8.4555 · DOI
- Jones, 1990, Proc. Natl. Acad. Sci. U. S. A., 87, 6117, 10.1073/pnas.87.16.6117 · DOI
- Wu, 1993, Proc. Natl. Acad. Sci. U. S. A., 90, 8891, 10.1073/pnas.90.19.8891 · DOI
- Sakamoto, 1993, Oncogene, 8, 1887
- Roy, 1992, Nucleic Acids Res., 20, 5753, 10.1093/nar/20.21.5753 · DOI
- Yoder, 1996, J. Biol. Chem., 271, 31092, 10.1074/jbc.271.49.31092 · DOI
- Christman, 1993, Carcinogenesis, 14, 551, 10.1093/carcin/14.4.551 · DOI
Cited by
Regulation of DNA Methyltransferase 1 by the pRb/E2F1 Pathway
McCabe, M. T., Davis, J. N., & Day, M. L. (2005) · Cancer Research · doi:10.1158/0008-5472.can-04-2158 · Cited by 172
Transposon-triggered innate immune response confers cancer resistance to the blind mole rat
Zhao, Y., Oreskovic, E., Zhang, Q., Lu, Q., Gilman, A., Lin, Y. S., He, J., Zheng, Z., Lu, J. Y., Lee, J., et al. (2021) · Nature Immunology · doi:10.1038/s41590-021-01027-8 · Cited by 99
Persaud, N. S., & Cates, H. M. (2023) · eneuro · doi:10.1523/eneuro.0109-21.2021 · Cited by 41
“…methyltransferase expression offer insight into to how these enzymes are able to respond to external stimuli to epigenetically modify gene expression in the CNS. Expression levels of DNMTs positively correlate to DNMT activity and thus to any global methylation trends observed (Slack et al., 1999).”
Background
Metadata
- Authors
- Slack, A., Cervoni, N., Pinard, M., & Szyf, M.
- Affiliations
- McGill University (CA)
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1999-04
- Volume
- 274
- Issue
- 15
- Pages
- 10105-10112
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2007287542
- Cited by
- 93
- References
- 1
- Citations by year
- 2023: 5 · 2022: 1 · 2021: 2 · 2018: 1 · 2017: 2 · 2016: 3 · 2015: 2 · 2014: 5 · 2013: 5 · 2012: 2
- FWCI
- 3.03
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Polyomavirus and related diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer-related gene regulation
- Keywords
- DNA methyltransferases, simian virus 40, T antigen, cell transformation, DNA methylation, mRNA stability, post-transcriptional regulation, carcinogenesis, soft agar colony formation
- MeSH terms
- Animals, Antigens, Viral, Tumor, Cell Transformation, Viral, Enzyme Induction, Mice, Inbred BALB C, Protein Processing, Post-Translational, RNA, Messenger, Simian virus 40, Transfection, DNA Modification Methylases, Up-Regulation, Oligonucleotides, Antisense, 3T3 Cells, DNA Methylation, Mice
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- This page
- CoChat. (2026). Citation check: DNA Methyltransferase Is a Downstream Effector of Cellular Transformation Triggered by Simian Virus 40 Large T Antigen. https://app.cochat.ai/papers/10.1074/jbc.274.15.10105
- The paper
- Slack, A., Cervoni, N., Pinard, M., & Szyf, M. (1999). DNA Methyltransferase Is a Downstream Effector of Cellular Transformation Triggered by Simian Virus 40 Large T Antigen. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.274.15.10105