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通过 MBD2/3-NuRD 复合物染色质重塑探索 E6 和 E7 癌蛋白在宫颈癌发生中的作用。

Exploring the Role of E6 and E7 Oncoproteins in Cervical Oncogenesis through MBD2/3-NuRD Complex Chromatin Remodeling.

机构信息

Stefan S. Nicolau Institute of Virology, Romanian Academy, 030304 Bucharest, Romania.

Pharmacology Department, National Institute for Chemical Pharmaceutical Research and Development, 031299 Bucharest, Romania.

出版信息

Genes (Basel). 2024 Apr 27;15(5):560. doi: 10.3390/genes15050560.

DOI:10.3390/genes15050560
PMID:38790189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11121560/
Abstract

BACKGROUND

Cervical cancer is among the highest-ranking types of cancer worldwide, with human papillomavirus (HPV) as the agent driving the malignant process. One aspect of the infection's evolution is given by epigenetic modifications, mainly DNA methylation and chromatin alteration. These processes are guided by several chromatin remodeling complexes, including NuRD. The purpose of this study was to evaluate the genome-wide binding patterns of the NuRD complex components (MBD2 and MBD3) in the presence of active HPV16 E6 and E7 oncogenes and to determine the potential of identified genes through an experimental model to differentiate between cervical precursor lesions, with the aim of establishing their utility as biomarkers.

METHODS

The experimental model was built using the CaSki cell line and shRNA for E6 and E7 HPV16 silencing, ChIP-seq, qRT-PCR, and Western blot analyses. Selected genes' expression was also assessed in patients.

RESULTS

Several genes have been identified to exhibit altered transcriptional activity due to the influence of HPV16 E6/E7 viral oncogenes acting through the MBD2/MBD3 NuRD complex, linking them to viral infection and cervical oncogenesis.

CONCLUSIONS

The impacted genes primarily play roles in governing gene transcription, mRNA processing, and regulation of translation. Understanding these mechanisms offers valuable insights into the process of HPV-induced oncogenesis.

摘要

背景

宫颈癌是全球排名最高的癌症类型之一，人乳头瘤病毒（HPV）是驱动恶性进程的主要因素。感染的一个演变方面是表观遗传修饰，主要是 DNA 甲基化和染色质改变。这些过程由几个染色质重塑复合物指导，包括 NuRD。本研究的目的是评估 NuRD 复合物成分（MBD2 和 MBD3）在存在活性 HPV16 E6 和 E7 致癌基因时的全基因组结合模式，并通过实验模型确定鉴定基因的潜力，以区分宫颈前病变，旨在确定它们作为生物标志物的效用。

方法

使用 CaSki 细胞系和 shRNA 构建实验模型，用于 HPV16 E6 和 E7 的沉默、ChIP-seq、qRT-PCR 和 Western blot 分析。还评估了患者中选定基因的表达。

结果

由于 HPV16 E6/E7 病毒致癌基因通过 MBD2/MBD3 NuRD 复合物的作用影响，一些基因的转录活性发生改变，将它们与病毒感染和宫颈癌变联系起来。

结论

受影响的基因主要在调控基因转录、mRNA 处理和翻译调控中发挥作用。了解这些机制为 HPV 诱导的致癌作用过程提供了有价值的见解。

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