A transcriptomic landscape of human papillomavirus 16 E6‐regulated gene expression and splicing events

Xu, Jianrong; Fang, Yifeng; Qin, Jiale; Chen, Xiaojing; Liang, Xiao; Xie, Xing; Lü, Weiguo

doi:10.1002/1873-3468.12486

Cited by 11 publications

(8 citation statements)

References 44 publications

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“…Several years later, another group demonstrated the splicing capabilities of HPV16 E6 overexpression in HPV-negative cells [ 103 ]. The changes to the transcriptome and splicing profile were compared upon the transient overexpression of HPV16 E6, and validated in clinical tissue samples.…”

Section: Mechanism Of E6 and E7 Regulating Cellular Pathwaysmentioning

confidence: 99%

High-Risk Human Papillomaviral Oncogenes E6 and E7 Target Key Cellular Pathways to Achieve Oncogenesis

Yeo-Teh

Ito

Jha

2018

IJMS

182

148

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Infection with high-risk human papillomavirus (HPV) has been linked to several human cancers, the most prominent of which is cervical cancer. The integration of the viral genome into the host genome is one of the manners in which the viral oncogenes E6 and E7 achieve persistent expression. The most well-studied cellular targets of the viral oncogenes E6 and E7 are p53 and pRb, respectively. However, recent research has demonstrated the ability of these two viral factors to target many more cellular factors, including proteins which regulate epigenetic marks and splicing changes in the cell. These have the ability to exert a global change, which eventually culminates to uncontrolled proliferation and carcinogenesis.

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Section: Mechanism Of E6 and E7 Regulating Cellular Pathwaysmentioning

confidence: 99%

High-Risk Human Papillomaviral Oncogenes E6 and E7 Target Key Cellular Pathways to Achieve Oncogenesis

Yeo-Teh

Ito

Jha

2018

IJMS

182

148

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“…The spectrum of signaling pathways reprogrammed in the "host" cell (keratinocyte) under the influence of HPV oncogenes E6 and E7 and depending on the life cycle of HPV (productive or unproductive, transforming infection) has been characterized [14] Spontaneously immortalized neonatal epidermal keratinocytes (NIKS) [15] Primary normal epidermal keratinocytes (NHEKs) [16] SV40 Т-antigen-immortalized embryonic kidney cells (HEK293T) [17] hTERT-immortalized keratinocytes of the oral cavity (NOKs)…”

Section: Referencesmentioning

confidence: 99%

RNA Sequencing and Cell Models of Virus-Associated Cancer (Review)

Kurmyshkina¹,

Bogdanova²,

Ковчур³

et al. 2022

Sovrem Tehnol Med

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The review summarizes findings from the studies based on the application of technologies for transcriptome analysis to modern cellular model systems of human papillomavirus-associated cancer (HPV) (cervical cancer, head and neck tumors). A diversity of three-dimensional cancer models, such as spheroids, organoids (organotypic cultures), explants, mouse xenografts, are addressed. Particular attention is paid to the use of patient-derived biomaterial for establishing short-term cultures of primary tumor cells, as well as generating multicomponent (heterocellular) systems that comprise, together with the tumor component, other elements of its microenvironment. A number of unique biological properties of HPV-induced neoplasia are discussed, which make generating cell models a unique task.The novel findings in the field of molecular mechanisms of the onset and progression of HPV-associated cancer achieved by using RNA sequencing are presented for each variant of the model systems. These findings are considered in regard to applied aspects of their use, in terms of the opportunities for preclinical testing of new drugs, personalized diagnostics and selection of individual, most effective treatment regimens. The issues of drug resistance development, molecular-cellular heterogeneity, epigenetic reprogramming, and the role of the stromal microenvironment are reviewed. The paper accentuates the problems related to the limitations of the applicability of a particular model system. The areas with a significant lagging behind in omics research of virus-associated cancer in comparison with other types of oncological pathology and possible causes of this lag are noted. The future prospects for the development of model systems of HPV-associated tumors in the field of high-tech tissue engineering, in particular, the use of bioprinting and microfluidic biochips, are also outlined. The combination of these techniques with the methods of whole genome profiling will significantly increase the translational potential of the described model cell systems.

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“…Two studies have shown that CELF3 may play a role in cancer. The upregulation of CELF3 is reported to be induced by HPV16 E6 and is thought to be crucial for downstream RNA splicing changes, such as exon skipping [94]. Furthermore, in patients with colorectal cancer metastasis, different patterns of expression and copy number variations are observed for CELF3.…”

Section: Other Celf Membersmentioning

confidence: 99%

CELF Family Proteins in Cancer: Highlights on the RNA-Binding Protein/Noncoding RNA Regulatory Axis

Aghdam

Jave‐Suárez

2021

IJMS

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Post-transcriptional modifications to coding and non-coding RNAs are unquestionably a pivotal way in which human mRNA and protein diversity can influence the different phases of a transcript’s life cycle. CELF (CUGBP Elav-like family) proteins are RBPs (RNA-binding proteins) with pleiotropic capabilities in RNA processing. Their responsibilities extend from alternative splicing and transcript editing in the nucleus to mRNA stability, and translation into the cytoplasm. In this way, CELF family members have been connected to global alterations in cancer proliferation and invasion, leading to their identification as potential tumor suppressors or even oncogenes. Notably, genetic variants, alternative splicing, phosphorylation, acetylation, subcellular distribution, competition with other RBPs, and ultimately lncRNAs, miRNAs, and circRNAs all impact CELF regulation. Discoveries have emerged about the control of CELF functions, particularly via noncoding RNAs, and CELF proteins have been identified as competing, antagonizing, and regulating agents of noncoding RNA biogenesis. On the other hand, CELFs are an intriguing example through which to broaden our understanding of the RBP/noncoding RNA regulatory axis. Balancing these complex pathways in cancer is undeniably pivotal and deserves further research. This review outlines some mechanisms of CELF protein regulation and their functional consequences in cancer physiology.

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A transcriptomic landscape of human papillomavirus 16 E6‐regulated gene expression and splicing events

Cited by 11 publications

References 44 publications

High-Risk Human Papillomaviral Oncogenes E6 and E7 Target Key Cellular Pathways to Achieve Oncogenesis

High-Risk Human Papillomaviral Oncogenes E6 and E7 Target Key Cellular Pathways to Achieve Oncogenesis

RNA Sequencing and Cell Models of Virus-Associated Cancer (Review)

CELF Family Proteins in Cancer: Highlights on the RNA-Binding Protein/Noncoding RNA Regulatory Axis

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