Chang Yao, Lan Yu-Yan, Hsiao Jenn-Ren, Chang Nan-Shan
National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Tainan 70456, Taiwan Graduate Institute of Basic Medical Science, Medical College, National Cheng Kung University, Tainan 70101, Taiwan
National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Tainan 70456, Taiwan Graduate Institute of Basic Medical Science, Medical College, National Cheng Kung University, Tainan 70101, Taiwan.
Exp Biol Med (Maywood). 2015 Mar;240(3):329-37. doi: 10.1177/1535370214561957. Epub 2014 Dec 7.
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.
含WW结构域的氧化还原酶(WWOX)是一种有充分文献记载的肿瘤抑制蛋白,可控制恶性细胞的生长、存活和转移。为了对抗WWOX的抑制作用,癌细胞已发展出许多策略,要么下调WWOX表达,要么使WWOX功能失活。在与某些病毒或细菌相关的癌症背景下,致癌病原体如何应对WWOX相对未知。在此,我们综述了最近的研究,这些研究展示了三种与癌症相关的病原体所采用的不同策略。幽门螺杆菌通过启动子高甲基化降低WWOX表达,这种表观遗传机制也在许多其他癌细胞中出现。WWOX有可能阻断由Tax诱导的经典核因子κB激活和肿瘤发生,Tax是人类T细胞白血病病毒的一种癌蛋白。Tax通过激活非经典核因子κB途径抑制WWOX表达,成功克服了这种阻断。另一方面,爱泼斯坦-巴尔病毒的潜伏膜蛋白2A与WWOX发生物理相互作用,并改变其功能以触发一条上调基质金属蛋白酶9和癌细胞侵袭的信号通路。关于WWOX与致癌微生物之间的多种相互作用,这些报道可能只是“冰山一角”。在这个方向上的进一步研究应该会扩展我们对感染驱动的肿瘤发生的理解。