Epigenetic mechanisms in virus-induced tumorigenesis

Poręba, Elżbieta; Broniarczyk, Justyna; Goździcka-Józefiak, Anna

doi:10.1007/s13148-011-0026-6

Cited by 46 publications

(46 citation statements)

References 158 publications

(236 reference statements)

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“…It also is tempting to speculate that p12, and p12-like proteins of other carlaviruses, may be considered as a latency factor (a latent protein) of this group of viruses and the viral-programmed induction of hyperplasia might be a way to delay the onset of HR (a type of programmed cell death) and to maintain the latent state of the virus infection (e.g., cell division without virus replication), as it has recently been shown that overexpression of Nt E2FB1 reduces programmed cell death induction in tobacco Bright Yellow-2 cells (Smetana et al, 2012). Moreover, it has been well documented that in animal/human viruses, some latent stages induce tumorogenesis (Poreba et al, 2011).…”

Section: Resultsmentioning

confidence: 99%

An RNA Virus-Encoded Zinc-Finger Protein Acts as a Plant Transcription Factor and Induces a Regulator of Cell Size and Proliferation in Two Tobacco Species

et al. 2013

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Plant viruses cause a variety of diseases in susceptible hosts. The disease symptoms often include leaf malformations and other developmental abnormalities, suggesting that viruses can affect plant development. However, little is known about the mechanisms underlying virus interference with plant morphogenesis. Here, we show that a C-4 type zinc-finger (ZF) protein, p12, encoded by a carlavirus (chrysanthemum virus B) can induce cell proliferation, which results in hyperplasia and severe leaf malformation. We demonstrate that the p12 protein activates expression of a regulator of cell size and proliferation, designated upp-L (upregulated by p12), which encodes a transcription factor of the basic/helix-loop-helix family sufficient to cause hyperplasia. The induction of upp-L requires translocation of the p12 protein into the nucleus and ZF-dependent specific interaction with the conserved regulatory region in the upp-L promoter. Our results establish the role of the p12 protein in modulation of host cell morphogenesis. It is likely that other members of the conserved C-4 type ZF family of viral proteins instigate reprogramming of plant development by mimicking eukaryotic transcriptional activators.

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Section: Resultsmentioning

confidence: 99%

An RNA Virus-Encoded Zinc-Finger Protein Acts as a Plant Transcription Factor and Induces a Regulator of Cell Size and Proliferation in Two Tobacco Species

et al. 2013

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“…The oncogenic potential of DNA viruses is variable, and their role in cancer pathogenesis is mediated through various mechanisms, including, for example, mutagenic integration into the host genome and expression of oncogenic viral proteins (2,3). The elucidation of such mechanisms has played a key role in enhancing our understanding of cancer pathogenesis even as novel aspects of DNA virus biology continue to be unraveled (4).…”

mentioning

confidence: 99%

Landscape of DNA Virus Associations across Human Malignant Cancers: Analysis of 3,775 Cases Using RNA-Seq

Khoury¹,

Tannir

Williams³

et al. 2013

J Virol

198

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Elucidation of tumor-DNA virus associations in many cancer types has enhanced our knowledge of fundamental oncogenesis mechanisms and provided a basis for cancer prevention initiatives. RNA-Seq is a novel tool to comprehensively assess such associations. We interrogated RNA-Seq data from 3,775 malignant neoplasms in The Cancer Genome Atlas database for the presence of viral sequences. Viral integration sites were also detected in expressed transcripts using a novel approach. The detection capacity of RNA-Seq was compared to available clinical laboratory data. Human papillomavirus (HPV) transcripts were detected using RNA-Seq analysis in head-and-neck squamous cell carcinoma, uterine endometrioid carcinoma, and squamous cell carcinoma of the lung. Detection of HPV by RNA-Seq correlated with detection by in situ hybridization and immunohistochemistry in squamous cell carcinoma tumors of the head and neck. Hepatitis B virus and Epstein-Barr virus (EBV) were detected using RNA-Seq in hepatocellular carcinoma and gastric carcinoma tumors, respectively. Integration sites of viral genes and oncogenes were detected in cancers harboring HPV or hepatitis B virus but not in EBV-positive gastric carcinoma. Integration sites of expressed viral transcripts frequently involved known coding areas of the host genome. No DNA virus transcripts were detected in acute myeloid leukemia, cutaneous melanoma, low-and high-grade gliomas of the brain, and adenocarcinomas of the breast, colon and rectum, lung, prostate, ovary, kidney, and thyroid. In conclusion, this study provides a large-scale overview of the landscape of DNA viruses in human malignant cancers. While further validation is necessary for specific cancer types, our findings highlight the utility of RNA-Seq in detecting tumor-associated DNA viruses and identifying viral integration sites that may unravel novel mechanisms of cancer pathogenesis.

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“…It has been found that genes encoded by oncogenic viruses such as HPV, Epstein-Barr virus, SV40, hepatitis B virus, and many others synthesize proteins which can interact with host epigenetic machinery leading to its deregulation. Studies have revealed that viral oncoproteins can indeed target the host genes such as DNMT, p53, pRB, and others, thereby altering the normal epigenetic mechanisms and acting as risk factors in the development and progression of cervical cancer [89][90][91] .…”

Section: Hpv and Other Pathogenic Infections Epigenetics And Cervicmentioning

confidence: 99%

Epigenomics, Pharmacoepigenomics, and Personalized Medicine in Cervical Cancer

Kabekkodu

Chakrabarty

Ghosh

et al. 2017

Public Health Genomics

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Epigenomics encompasses the study of genome-wide changes in DNA methylation, histone modifications and noncoding RNAs leading to altered transcription, chromatin structure, and posttranscription RNA processing, respectively, resulting in an altered rate of gene expression. The role of epigenetic modifications facilitating human diseases is well established. Previous studies have identified histone and cytosine code during normal and pathological conditions with special emphasis on how these modifications regulate transcriptional events. Recent studies have also mapped these epigenetic modification and pathways leading to carcinogenesis. Discovery of drugs that target proteins/enzymes in the epigenetic pathways may provide better therapeutic opportunities, and identification of such modulators for DNA methylation, histone modifications, and expression of noncoding RNAs for several cancer types is underway. In this review, we provide a detailed description of recent developments in the field of epigenetics and its impact on personalized medicine to manage cervical cancer.

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Epigenetic mechanisms in virus-induced tumorigenesis

Cited by 46 publications

References 158 publications

An RNA Virus-Encoded Zinc-Finger Protein Acts as a Plant Transcription Factor and Induces a Regulator of Cell Size and Proliferation in Two Tobacco Species

An RNA Virus-Encoded Zinc-Finger Protein Acts as a Plant Transcription Factor and Induces a Regulator of Cell Size and Proliferation in Two Tobacco Species

Landscape of DNA Virus Associations across Human Malignant Cancers: Analysis of 3,775 Cases Using RNA-Seq

Epigenomics, Pharmacoepigenomics, and Personalized Medicine in Cervical Cancer

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