致瘤性HPV感染异常调节组蛋白H3剪切

Jorge SANDOVAL-BASILIO, Sofia L. Alcaraz-Estrada
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引用次数: 0

摘要

在各种病原体的感染过程中,表观遗传改变的积累导致基因表达或病毒再激活的变化。致瘤性人乳头瘤病毒(HPV)失调各种表观遗传机制。组蛋白H3剪切受损构成宫颈癌的表观遗传机制。然而,H3剪接受损是否作为HPV感染的主要影响发生,还是由于大量改变而导致宫颈癌的结果尚不清楚。使用对癌症病理呈阴性,但对致癌HPV呈阳性和阴性的人类宫颈样本,我们能够确定与致癌HPV阴性子宫颈相比,致癌HPV阳性子宫颈中的H3剪接较低。这些结果表明,以前在宫颈癌中观察到的低H3剪切可能是致癌HPV感染的主要影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oncogenic HPV Infection Dysregulates Histone H3 Clipping
, Abstract During infection by various pathogens, there is an accumulation of epigenetic alterations that lead to changes in gene expression or viral reactivation. Oncogenic Human Papillomavirus (HPV) dysregulate various epigenetic mechanisms. Impaired histone H3 clipping constitutes an epigenetic mechanism in cervical cancer. However, if the impaired H3 clipping occurred as a primary effect of the HPV infection or if is a consequence of cervical carcinogenesis due to the high number of alterations is unknown. Using human cervical samples with negative pathology to cancer, but positive and negative to oncogenic HPV, we were able to identify that H3 clipping was low in the positive oncogenic HPV cervix compared to the negative oncogenic HPV cervix. These results suggest that low H3 clipping previously observed in cervical cancer may be a primary effect of oncogenic HPV infection.
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