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A paradigm for post-embryonic Oct4 re-expression: E7-induced hydroxymethylation regulates Oct4 expression in cervical cancer

ABSTRACT: A paradigm for post-embryonic Oct4 re-expression: E7-induced hydroxymethylation regulates Oct4 expression in cervical cancer

PROVIDER: PRJNA1043606 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26899025.fastq.gz	Fastqsanger.gz
	SRR26899025_1.fastq.gz	Fastqsanger.gz
	SRR26899025_2.fastq.gz	Fastqsanger.gz
	SRR26899026.fastq.gz	Fastqsanger.gz
	SRR26899026_1.fastq.gz	Fastqsanger.gz

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A paradigm for post-embryonic Oct4 re-expression: E7-induced hydroxymethylation regulates Oct4 expression in cervical cancer

Project description:The Octamer-binding transcription factor-4 (Oct4) is upregulated in different malignancies, yet a paradigm for mechanisms of Oct4 post-embryonic re-expression is inadequately understood. In cervical cancer, Oct4 expression is higher in HPV-related than HPV-unrelated cervical cancers and this upregulation correlates with the expression of the E7 oncogene. We have reported that E7 affects the Oct4-transcriptional output and Oct4-related phenotypes in cervical cancer, however, the underlying mechanism remains elusive. Here, we characterize the Oct4-protein interactions in cervical cancer cells and reveal that Methyl-binding proteins (MBD2 and MBD3), are determinants of Oct4 driven transcription. E7 triggers MBD2 downregulation and TET1 upregulation, thereby disrupting the methylation status of the Oct4 gene. This coincides with an increase in the total DNA hydroxymethylation leading to the re-expression of Oct4 in cervical cancer and likely affecting broader transcriptional patterns. Our findings reveal a previously unreported mechanism by which the E7 oncogene can regulate transcription by increasing DNA hydroxymethylation and lowering the barrier to cellular plasticity during carcinogenesis.

2023-12-11 | GSE248367 | GEO

Oct4 re-expression in cervical cancer

Project description:E7 modulates Oct4 re-expression in cervical cancer

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HPV E7 binds Oct4 and regulates its activity in HPV-associated cervical cancers.

Project description:Human papillomavirus E7 binds Oct4 and regulates its activity in HPV-associated cervical cancers.

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GENE EXPRESSION PROFILE REGULATED BY THE HPV16-E7 ONCOPROTEIN AND ESTRADIOL IN CERVICAL TISSUE

Project description:The HPV16-E7 oncoprotein and 17β-estradiol are import factors for the induction of premalignant lesions and cervical cancer. The study of these factors is crucial for a better understanding of cervical tumorigenesis. In this study, we performed a microarray analysis to obtain a global gene expression profile induced by both, HPV16-E7 and 17β-estradiol in cervical tissue of K14E7 transgenic mice. We found that 17β-estradiol is the main cause of the up-regulation of a large number of cellular genes involved in the immune response whereas E7 oncoprotein mainly affects the cellular metabolism. Our microarray data also shows some novel differentially expressed genes that were not previously reported in cervical cancer. The identification of these genes, regulated by E7 and 17β-estradiol, provides the basis for further studies on their role in cervical carcinogenesis.

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GENE EXPRESSION PROFILE REGULATED BY THE HPV16-E7 ONCOPROTEIN AND ESTRADIOL IN CERVICAL TISSUE

Project description:The HPV16-E7 oncoprotein and 17Î²-estradiol are import factors for the induction of premalignant lesions and cervical cancer. The study of these factors is crucial for a better understanding of cervical tumorigenesis. In this study, we performed a microarray analysis to obtain a global gene expression profile induced by both, HPV16-E7 and 17Î²-estradiol in cervical tissue of K14E7 transgenic mice. We found that 17Î²-estradiol is the main cause of the up-regulation of a large number of cellular genes involved in the immune response whereas E7 oncoprotein mainly affects the cellular metabolism. Our microarray data also shows some novel differentially expressed genes that were not previously reported in cervical cancer. The identification of these genes, regulated by E7 and 17Î²-estradiol, provides the basis for further studies on their role in cervical carcinogenesis. 15 Mouse Gene 1.0 ST Affymetrix microarrays were used to analyze gene expression of cervical tissue from K14E7 hemizygote and nontransgenic FvB control virgin female untreated and treated mice. Briefly, one-month virgin female transgenic and nontransgenic mice were implanted in the dorsal skin with continuous release pellets delivering 0.05 mg of17-Î² estradiol over 60 days. As control samples we used K14E7 and FvB untreated mice. For the microarray analysis we used triplicates for each group (3 treated K14E7 mice, 3 treated FvB mice, 3 untreated K14E7 mice, 3 untreated FvB mice).

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Paradigm Test Set

Project description:Paradigm Test Set

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Project description:Human papillomavirus (HPV) genome integration into the host genome, blocking E2 expression and leading to overexpression of E6 and E7 viral oncogenes, is considered a major step in cervical cancer development. In high-risk HPVs, E6 and E7 oncogenes are expressed as a bicistronic pre-mRNA, with alternative splicing producing the ultimate mRNAs required for E6 and E7 translation. Given the number of alternative donor and acceptor splicing sites, ten E6/E7 different alternative transcripts might be formed for HPV16 and three for HPV18, although only six isoforms have been previously reported for HPV16. In the present work, we employ high-throughput sequencing of invasive cervical cancer transcriptome (RNA-Seq) to characterize the expression of the HPV genome in 24 invasive cervical cancers associated with HPV16 and HPV18 single infections. Based on high-resolution transcriptional maps, we herein report three viral gene expression patterns which might be associated with the presence of the viral genome in episomal and/or integrated stages. Alternative mRNAs splicing isoforms coding for E6 and E7 oncoproteins were characterized and quantified, and two novel isoforms were identified. Three major isoforms (E6*I, E6*II, and E6+E7) were detected for HPV16 and two for HPV18 (E6*I and E6+E7). Minor transcript isoforms, including the novel ones, were very rare in some tumor samples or were not detected. Our data suggested that minor transcript isoforms of E6/E7 do not play a relevant role in cervical cancer.

2019-08-06 | GSE91065 | GEO

Gene expression analysis of cervical cancer cells transfected with siRNAs against either HPV E6 or E6/E7

Project description:The study aimed to explore HPV E7-specific pathways in cervical cancer cells.

2024-08-25 | GSE274812 | GEO

Bartonella birtlesii E7 strain:E7

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