Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Downstream targets of ATR in CIN612 HPV-positive cells

ABSTRACT: Downstream targets of ATR in CIN612 HPV-positive cells

PROVIDER: PRJNA597129 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10752866.fastq.gz	Fastqsanger.gz
	SRR10752867.fastq.gz	Fastqsanger.gz
	SRR10752868.fastq.gz	Fastqsanger.gz
	SRR10752869.fastq.gz	Fastqsanger.gz
	SRR10752870.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Downstream targets of ATR in CIN612 HPV-positive cells

Project description:High-risk human papillomaviruses (HPVs) constitutively activate the ataxia telangiectasia and Rad3-related (ATR) DNA damage response pathway for their replication. Although ATR has many reported functions, knowledge of how it regulates viral replication is limited. Most studies regarding ATR function focus on its roles in cell survival and initiation of DNA damage response. In this study, we examined whether the transcriptional regulatory properties directed by ATR are critical for HPV pathogenesis, and if so which downstream targets are important. Using RNA-seq approaches, we observed that ATR knockdown increases expression of many inflammatory genes. This mechanism is dependent on the p62/GATA4 signaling pathway.

2020-07-27 | GSE142482 | GEO

Downstream Target Screening of TopBP1 in differentiated HPV-positive keratinocytes

Project description:Downstream Target Screening of TopBP1 in differentiated HPV-positive keratinocytes

| PRJNA503141 | ENA

MicroRNA analysis in HPV-positive and HPV-negative cervical cancer cell lines

Project description:Persistent infection by high-risk human papillomaviruses (HPVs) is associated with the development of cervical cancer and a subset of anogenital and head and neck squamous cell carcinomas. Abnormal expression of cellular microRNAs (miRNAs) plays an important role in the development of cancer, including HPV-related tumors. MiRNA expression profile was investigated by microrray analysis in the HPV-positive cervical cancer cell lines SiHa (HPV16-positive cell line derived from a cervical squamous cell carcinoma), CaSki (HPV16-positive cell line derived from a metastatic cervical epidermoid carcinoma), and HeLa (HPV18-positive cell line derived from a cervical adenocarcinoma) and compared with primary HFKs and C33a (HPV-negative cervical cell line).

2018-01-16 | E-MTAB-6361 | biostudies-arrayexpress

Whole-genome shallow-sequencing of HPV-positive and HPV-negative vulvar lesions

Project description:Identification of copy number alterations of HPV-positive and HPV-negative vulvar squamous cell carcinomas (VSCC) and vulvar intraepithelial neoplasias (VIN), with special focus on VIN with and without VSCC, the latter group being defined as VIN with no VSCC development during >10 year follow-up.

2018-07-01 | E-MTAB-6113 | biostudies-arrayexpress

Identification of downstream targets of the human papillomavirus E6 and E7 oncoproteins by RNA interference

Project description:Specific types of human papillomaviruses (HPVs) cause cervical cancer, the second most common tumor in females worldwide. Both cellular transformation and the maintenance of the oncogenic phenotype of HPV-positive tumor cells are linked to the expression of the viral E6 and E7 oncogenes. In order to identify downstream cellular target genes for the viral oncoproteins, we silenced endogenous E6 and E7 expression in HPV-positive HeLa cells by RNA interference (RNAi). Subsequently, we assessed changes of the cellular transcriptome by genome-wide microarray analysis. We identified, 648 genes wich were either downregulated (360 genes) or upregulated (288 genes) upon inhibition of E6/E7 expression. A large fraction of these genes is involved in tumour-relevant processes, such as apoptosis control, cell cycle regulation, or spindle formation. Others may represent novel cellular targets for the HPV oncogenes, such as a large group of C-MYC-associated genes involved in RNA splicing. Keywords: siRNA mediated knockdown

2007-07-01 | GSE6926 | GEO

Identification of miR-154 downstream targets

Project description:Identification of miR-154 downstream targets

| PRJNA593019 | ENA

Whole-genome shallow-sequencing of HPV-positive and HPV-negative vulvar lesions

Project description:Whole-genome shallow-sequencing of HPV-positive and HPV-negative vulvar lesions

| PRJEB22906 | ENA

Pleiotropic effects of Metformin on the chemotherapy response of HPV-positive cancer cells

Project description:Metformin has been shown to downregulate viral E6/E7 expression in HPV-positive cancer cells. However, Metformin does not induce cellular senescence, which is observed upon E6/E7 repression by RNA interference. Here we compare mass spectrometry-based proteome analyses of Metformin-treated SiHa cells (previously deposited to the ProteomeXchange Consortium with data set identifier PXC011095) with proteome analyses of SiHa cells transfected with si16E6/E7 or control siRNA (siCtrl-1) and grown for 72 hours to evaluate differences in the cell cycle regulation of HPV-positive cancer cells upon E6/E7 repression by Metformin or siE6/E7.

2025-06-17 | PXD061861 | Pride

Genomic analysis of HPV positive versus HPV negative esophageal adenocarcinoma

Project description:High-risk human papillomavirus (hr-HPV) has been implicated in a subset of patients with esophageal adenocarcinoma (EAC). We therefore hypothesized that HPV associated EAC may have distinct genomic aberrations compared with viral negative esophageal cancer as shown in Head and Neck cancer and cervical cancer. Whole exome sequencing (WES) was performed to explore the mutational landscape and potential molecular signature of HPV positive versus HPV negative EAC, which includes four hr-HPV-positive and 8 HPV-negative treatment naive fresh-frozen EAC tissue specimens and matched normal tissues.

| EGAS00001001340 | EGA

c-MYC-dependent transcriptional inhibition of autophagy is implicated in Cisplatin sensitivity in HPV-positive Head and Neck Cancer

Project description:Autophagy is important for removal, degradation and recycling of damaged organelles, proteins, and lipids through the degradative action of lysosomes. In addition to its catabolic function, autophagy is important in cancer and viral-mediated tumorigenesis, including Human Papillomavirus (HPV) positive cancers. HPV infection is a major risk factor in a subset of Head and Neck Cancer (HNC), for which no targeted therapies are currently available. Herein, we assessed autophagy function in HPV-positive HNC. We showed that HPV-positive HNC cells presented a transcriptional and functional impairment of autophagic process compared to HPV-negative cells, which was reactivated by knocking-down HPV E6/E7 oncoproteins, the drivers of cellular transformation. We found that the oncoprotein c-MYC was stabilized and triggered in HPV-positive cell lines. This resulted in the reduced binding of the MiT/TFE transcription factors to their autophagy targets due to c-MYC competition. Thus, knock-down of c-MYC induced the upregulation of autophagic and lysosomal genes in HPV-positive HNC cells, as well as the increase of autophagic markers at the protein level. Moreover, HPV oncoprotein E7 upregulated the expression of the phosphatase inhibitor CIP2A, accounting for c-MYC upregulation and stability in HPV+ HNC cells. CIP2A mRNA expression negatively correlated with autophagy gene expression in tumor tissues from HNC patients, showing, for the first time, its implication in a transcriptional autophagic context. Both CIP2A and c-MYC knock-down, as well as pharmacological downregulation of c-MYC, resulted in increased resistance to Cisplatin treatment. Our results not only show a novel way by which HPV oncoproteins manipulate the host machinery, but also provide more insights on the role of autophagy in chemoresistance, with possible implications for targeted HPV-positive HNC therapy.

2023-11-08 | GSE235662 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data