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Connivance complicity or collusion? The role of noncoding RNAs in promoting gammaherpesvirus tumorigenesis.

机译:纵容共谋或共谋?非编码RNA在促进γ疱疹病毒肿瘤发生中的作用。

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摘要

EBV and KSHV are etiologic agents of multiple types of lymphomas and carcinomas. The frequency of EBV+ or KSHV+ malignancies arising in immunocompromised individuals reflects the intricate evolutionary balance established between these viruses and their immunocompetent hosts. However, the specific mechanisms by which these pathogens drive tumorigenesis remain poorly understood. In recent years an enormous array of cellular and viral noncoding RNAs (ncRNAs) have been discovered, and host ncRNAs have been revealed as contributory factors to every single cancer hallmark cellular process. As new evidence emerges that gammaherpesvirus ncRNAs similarly alter host cell pathways, viral factors dysregulate host ncRNA expression, and novel viral ncRNAs have yet to be discovered, we examine the contribution of small, non-miRNA ncRNAs and long ncRNAs in gammaherpesvirus tumorigenesis.
机译:EBV和KSHV是多种类型的淋巴瘤和癌的病因。免疫功能低下的个体中出现的EBV + 或KSHV + 恶性肿瘤的频率反映了这些病毒与其免疫能力强的宿主之间建立的复杂的进化平衡。但是,这些病原体驱动肿瘤发生的具体机制仍然知之甚少。近年来,已发现大量细胞和病毒非编码RNA(ncRNA),并且宿主ncRNA已被揭示为每个癌症标志性细胞过程的促成因素。随着新证据的出现,γ疱疹病毒ncRNA同样改变宿主细胞途径,病毒因子失调宿主ncRNA表达,并且尚未发现新型病毒ncRNA,我们研究了小型,非miRNA ncRNA和长ncRNA在γ疱疹病毒肿瘤发生中的作用。

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