Strategies of oncogenic microbes to deal with WW domain-containing oxidoreductase

WW domain-containing oxidoreductase (WWOX) is a well-documented tumor suppressor protein that controls growth, survival, and metastasis of malignant cells. To counteract WWOX’s suppressive effects, cancer cells have developed many strategies either to downregulate WWOX expression or to functionally...

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Bibliographic Details
Published in:Experimental biology and medicine (Maywood, N.J.) N.J.), 2015-03, Vol.240 (3), p.329-337
Main Authors: Chang, Yao, Lan, Yu-Yan, Hsiao, Jenn-Ren, Chang, Nan-Shan
Format: Article
Language:English
Subjects:
Carcinogenesis
Deltaretrovirus - physiology
Down-Regulation - physiology
Helicobacter pylori - physiology
Herpesvirus 4, Human - physiology
Humans
Minireviews
Oxidoreductases - physiology
Signal Transduction - physiology
Tumor Suppressor Proteins - physiology
WW Domain-Containing Oxidoreductase
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Summary:WW domain-containing oxidoreductase (WWOX) is a well-documented tumor suppressor protein that controls growth, survival, and metastasis of malignant cells. To counteract WWOX’s suppressive effects, cancer cells have developed many strategies either to downregulate WWOX expression or to functionally inactivate WWOX. Relatively unknown is, in the context of those cancers associated with certain viruses or bacteria, how the oncogenic pathogens deal with WWOX. Here we review recent studies showing different strategies utilized by three cancer-associated pathogens. Helicobactor pylori reduces WWOX expression through promoter hypermethylation, an epigenetic mechanism also occurring in many other cancer cells. WWOX has a potential to block canonical NF-κB activation and tumorigenesis induced by Tax, an oncoprotein of human T-cell leukemia virus. Tax successfully overcomes the blockage by inhibiting WWOX expression through activation of the non-canonical NF-κB pathway. On the other hand, latent membrane protein 2A of Epstein–Barr virus physically interacts with WWOX and redirects its function to trigger a signaling pathway that upregulates matrix metalloproteinase 9 and cancer cell invasion. These reports may be just “the tip of the iceberg” regarding multiple interactions between WWOX and oncogenic microbes. Further studies in this direction should expand our understanding of infection-driven oncogenesis.
ISSN:1535-3702
1535-3699
DOI:10.1177/1535370214561957