JC virus existence in Chinese gastrointestinal carcinomas

Wang, Jianping; Wang, Zuozhou; Zheng, Yushuang; Pu, Xia; Yang, Xianghong; Liu, Yunpeng; Takano, Yasuo; Zheng, Haixue

doi:10.3892/ol.2012.627

Cited by 10 publications

(8 citation statements)

References 27 publications

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“…However, during the last decade, an increasing number of studies provide clear evidence for the role of JCV in brain and gastrointestinal tract tumorigenesis. More than 6 independent laboratories have detected JCV and studied the mechanisms behind its oncogenic role in colon cancer [10] , [23] – [30] . Interestingly, patients with advanced colorectal neoplasia have significantly higher JCV antibody titers than healthy controls, suggesting an association between viral load or reactivation and risk of transformation [54] .…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, Bofill-Mas, et al showed that viral particles isolated from sewage remained intact after treatment at a pH of 1 for 30 minutes, indicating that ingestion of contaminated water or food may be sufficient for JCV infection of the gastrointestinal tract [20] . Many studies since, have demonstrated the presence of JCV genomic sequences and the expression of T-Antigen in tissues from gastrointestinal tumors, including esophageal carcinoma [11] , gastric carcinoma [12] , [21] , [22] , sporadic adenomatous polyps [23] , and colorectal adenocarcinomas [10] , [24] – [30] .…”

Section: Introductionmentioning

confidence: 99%

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Activation of c-Myc and Cyclin D1 by JCV T-Antigen and β-Catenin in Colon Cancer

et al. 2014

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During the last decade, mounting evidence has implicated the human neurotropic virus JC virus in the pathology of colon cancer. However, the mechanisms of JC virus-mediated oncogenesis are still not fully determined. One candidate to mediate these effects is the viral early transcriptional product T-Antigen, which has the ability to inactivate cell cycle regulatory proteins such as p53. In medulloblastomas, T-Antigen has been shown to bind the Wnt signaling pathway protein β-catenin; however, the effects of this interaction on downstream cell cycle regulatory proteins remain unknown. In light of these observations, we investigated the association of T-Antigen and nuclear β-catenin in colon cancer cases and the effects of this complex in the activation of the transcription and cell cycle regulators c-Myc and Cyclin D1 in vitro. Gene amplification demonstrated the presence of viral sequences in 82.4% of cases and we detected expression of T-Antigen in 64.6% of cases by immunohistochemistry. Further, we found that T-Antigen and β-catenin co-localized in the nuclei of tumor cells and we confirmed the physical binding between these two proteins in vitro. The nuclear presence of T-Antigen and β-catenin resulted in the significant enhancement of TCF-dependent promoter activity and activation of the β-catenin downstream targets, c-Myc and Cyclin D1. These observations provide further evidence for a role of JCV T-Antigen in the dysregulation of the Wnt signaling pathway and in the pathogenesis of colon cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Activation of c-Myc and Cyclin D1 by JCV T-Antigen and β-Catenin in Colon Cancer

et al. 2014

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“…In previous studies, we established transgenic mice and found that T antigen induced lens tumors and lung cancer ( Gou et al, 2015 ; Noguchi et al, 2013 ). Recently, JCV was demonstrated to correlate with colorectal, gastric, prostatic, and esophageal cancers, brain tumors, lung cancer, and B cell lymphomas ( Del Valle et al, 2005 ; Zheng et al, 2007a ; Murai et al, 2007 ; Kutsuna et al, 2008 ; Ramamoorthy et al, 2011 ; Shen et al, 2011 ; Wang et al, 2012 ; Noguchi et al, 2013 ; Anzivino et al, 2015 ; MalekpourAfshar et al, 2016 ). The oncogenesis of JCV mainly centers on T antigen.…”

Section: Introductionmentioning

confidence: 99%

The Oncogenic Roles of JC Virus T Antigen in Breast Carcinogenesis

Zheng

Ying

Cui

et al. 2021

Front. Mol. Biosci.

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Purpose: JC virus (JCV) infects 80–90% of the population and results in progressive multifocal leukoencephalopathy upon immunodeficiency. The study aimed to pathologically clarify the oncogenic roles of T antigen in human breast cancers.Methods: Breast cancer, dysplasia, and normal tissues were examined for T antigen of JCV by nested and real-time PCR. The positive rate or copy number of T antigen was compared with clinicopathological parameters of breast cancer. JCV existence was morphologically detected by immunohistochemistry and in situ PCR. T antigen was examined by Western blot using frozen samples of breast cancer and paired normal tissues.Results: According to nested PCR, the positive rate of breast ductal or lobular carcinoma was lower than that of normal tissue (p < 0.05). T antigen existence was negatively correlated with E-cadherin expression and triple-negative breast cancer (p < 0.05), but positively correlated with lymph node metastasis and estrogen receptor and progestogen receptor expression (p < 0.05). Quantitative PCR showed that JCV copies were gradually decreased from normal, dysplasia to cancer tissues (p < 0.05). JCV T antigen copy number was lower in ductal adenocarcinoma than in normal tissue (p < 0.05), in line with in situ PCR and immunohistochemistry. JCV copies were negatively correlated with tumor size and E-cadherin expression (p < 0.05), but positively correlated with G grading of breast cancer (p < 0.05). Western blot also indicated weaker T antigen expression in breast cancer than normal tissues (p < 0.05).Conclusion: JCV T antigen might play an important role in breast carcinogenesis. It can be employed as a molecular marker for the differentiation and aggressive behaviors of breast cancer.

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“…As in brain tumors, the study by Enam demonstrated that the JCPyV genomic sequences were amplified from tumor cells micro-dissected from the tissue using laser capture. Such studies have been successfully reproduced in different ethnic groups of people and in countries al around the world, including Japan (165), China (166, 167), Taiwan (168), Israel (169), Portugal (170), and Tunisia (171). The multiple studies on colon cancer have also been important for several reasons; they have shown that preneoplastic polyps and adenocarcinomas contain up to 20 × 10 3 viral copies per microgram of DNA, while adjacent colonic mucosa and normal colon have only a low viral load (172), implicating JCPyV in the process of neoplastic transformation.…”

Section: Introductionmentioning

confidence: 99%

Human Polyomavirus JCPyV and Its Role in Progressive Multifocal Leukoencephalopathy and Oncogenesis

Valle

Piña‐Oviedo

2019

Front. Oncol.

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The human neurotropic virus JCPyV, a member of the Polyomaviridiae family, is the opportunistic infectious agent of Progressive Multifocal Leukoencephalopathy (PML), a fatal disease seen in severe immunosuppressive conditions and, during the last decade, in patients undergoing immunotherapy. JCPyV is a ubiquitous pathogen with up to 85% of the adult population word-wide exhibiting antibodies against it. Early experiments demonstrated that direct inoculation of JCPyV into the brain of different species resulted in the development of brain tumors and other neuroectodermal-derived neoplasias. Later, several reports showed the detection of viral sequences in medulloblastomas and glial tumors, as well as expression of the viral protein T-Antigen. Few oncogenic viruses, however, have caused so much controversy regarding their role in the pathogenesis of brain tumors, but the discovery of new Polyomaviruses that cause Merkel cell carcinomas in humans and brain tumors in racoons, in addition to the role of JCPyV in colon cancer and multiple mechanistic studies have shed much needed light on the role of JCPyV in cancer. The pathways affected by the viral protein T-Antigen include cell cycle regulators, like p53 and pRb, and transcription factors that activate pro-proliferative genes, like c-Myc. In addition, infection with JCPyV causes chromosomal damage and T-Antigen inhibits homologous recombination, and activates anti-apoptotic proteins, such as Survivin. Here we review the different aspects of the biology and physiopathology of JCPyV.

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JC virus existence in Chinese gastrointestinal carcinomas

Cited by 10 publications

References 27 publications

Activation of c-Myc and Cyclin D1 by JCV T-Antigen and β-Catenin in Colon Cancer

Activation of c-Myc and Cyclin D1 by JCV T-Antigen and β-Catenin in Colon Cancer

The Oncogenic Roles of JC Virus T Antigen in Breast Carcinogenesis

Human Polyomavirus JCPyV and Its Role in Progressive Multifocal Leukoencephalopathy and Oncogenesis

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