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MicroRNA sequencing and Novel HPV miRNA discovery in HPV cell lines and human tissue samples

ABSTRACT: Human papillomaviruses (HPV) preferentially infect keratinocytes of mucous membranes or skin and cause numerous benign and malignant lesions at different anatomical locations. A number of DNA viruses encode their own miRNAs as well. To date, no studies have been able to validate viral miRNAs in papillomavirus infected cells using standard sequencing or next generation sequencing techniques. We sequenced small RNA (sRNA) libraries of two HPV 16 immortalized cell lines, HPK IA and HPK II, and ten formalin fixed paraffin embedded (FFPE) tissue samples from HPV infected cervical epithelium by SOLiD 4 technology. We used the miRSeqNovel software, to predict novel miRNAs and their likely pre-miRNAs. We further validated (qRT-PCR, northern blotting and in situ hybridization) the candidate miRNAs in a number of tissue samples from HPV associated cervical disease and also in HPV 16 positive cell lines CaSki and SiHa. Altogether nine candidate microRNAs were identified. The expression of four out of five studied miRNAs was confirmed in human tissue or human epithelial cell lines harboring HPV 16.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42380 | GEO | 2013/08/18

SECONDARY ACCESSION(S): PRJNA181288

REPOSITORIES: GEO

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MicroRNA sequencing and Novel HPV miRNA discovery in HPV cell lines and human tissue samples

Project description:Human papillomaviruses (HPV) preferentially infect keratinocytes of mucous membranes or skin and cause numerous benign and malignant lesions at different anatomical locations. A number of DNA viruses encode their own miRNAs as well. To date, no studies have been able to validate viral miRNAs in papillomavirus infected cells using standard sequencing or next generation sequencing techniques. We sequenced small RNA (sRNA) libraries of two HPV 16 immortalized cell lines, HPK IA and HPK II, and ten formalin fixed paraffin embedded (FFPE) tissue samples from HPV infected cervical epithelium by SOLiD 4 technology. We used the miRSeqNovel software, to predict novel miRNAs and their likely pre-miRNAs. We further validated (qRT-PCR, northern blotting and in situ hybridization) the candidate miRNAs in a number of tissue samples from HPV associated cervical disease and also in HPV 16 positive cell lines CaSki and SiHa. Altogether nine candidate microRNAs were identified. The expression of four out of five studied miRNAs was confirmed in human tissue or human epithelial cell lines harboring HPV 16. Small RNA (sRNA) libraries of two HPV 16 immortalized cell lines, HPK IA and HPK II, and ten formalin fixed paraffin embedded (FFPE) tissue samples from HPV infected cervical epithelium, were made according to SOLiD sequencing instructions.

2013-08-18 | E-GEOD-42380 | biostudies-arrayexpress

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

HPV cell lines and HPV tissue MicroRNA SOLiD sequencing

Project description:Human papillomaviruses (HPV) preferentially infect keratinocytes of mucous membranes or skin and cause numerous benign and malignant lesions at different anatomical locations. We sequenced small RNA (sRNA) libraries of two HPV 16 immortalized cell lines and ten formalin fixed paraffin embedded (FFPE) tissue samples from HPV infected cervical epithelium by SOLiD 4 technology.

2020-06-30 | GSE62239 | GEO

Expression data from HPV(-) and HPV(+) squamous cell carcinoma cell lines

Project description:Oncogenic human papillomaviruses (HPVs) are associated with nearly all carcinomas of the uterine cervix and have also become an increasingly important factor in the etiology of a subset of oropharyngeal tumors. HPV-associated head and neck cancers (HNSCCs) have a distinct risk profile and appreciate a prognostic advantage compared to HPV-negative HNSCC. We analyzed the genome-wide expression patterns in two HPV(+) and two HPV(-) squamous cell carcinoma (SCC) cell lines. The Affymetrix Human Genome U133 Plus 2.0 Array platform was used to assess genome-wide expression differences between the HPV(+) and HPV(-) cell lines utilizing the RMA normalization package available for R. Cell lines analyzed: UM-SCC-4, UM-SCC-47, UM-SCC-74A, and CaSki.

2010-12-01 | E-GEOD-24089 | biostudies-arrayexpress

Expression data from HPV(-) and HPV(+) squamous cell carcinoma cell lines

2010-12-01 | GSE24089 | GEO

A ubiquitin variant-based affinity approach selectively identifies substrates of the ubiquitin ligase E6AP in complex with HPV-11 E6 or HPV-16 E6

Project description:The E6 protein of both mucosal high risk human papillomaviruses (HPVs) such as HPV-16, which have been causally associated with malignant tumors, and low risk HPVs such as HPV-11, which cause the development of benign tumors, interacts with the cellular E3 ubiquitin ligase E6AP. This indicates that both HPV types employ E6AP to organize the cellular proteome to viral needs. However, while several substrate proteins of the high risk E6-E6AP complex are known, e.g. the tumor suppressor p53, potential substrates of the low risk E6-E6AP complex remain largely elusive. Here, we report on an affinity-based enrichment approach that enables the targeted identification of potential substrate proteins of the different E6-E6AP complexes by a combination of E3-selective ubiquitination in whole cell extracts and high-resolution mass spectrometry. The basis for the selectivity of this approach is the use of a ubiquitin variant that is efficiently used by the E6-E6AP complexes for ubiquitination, but not by E6AP alone. By this approach, we identified approximately 190 potential substrate proteins for low risk HPV-11 E6 as well as high risk HPV-16 E6. Moreover, subsequent validation experiments in vitro and within cells with selected substrate proteins demonstrate the potential of our approach. In conclusion, our data represent a reliable repository for potential substrates of the HPV-16 and HPV-11 E6 proteins in complex with E6AP.

2020-08-31 | PXD020660 | Pride

HPV E6 Impairs Translesion Synthesis by Blocking POLη Induction

Project description:Many DNA tumor viruses inhibit or repurpose host DNA repair pathways to evade viral defense mechanisms or promote their own replication. High risk genus α human papillomaviruses (α-HPVs) express two versatile oncogenes (α-HPV E6 and E7) that use both approaches simultaneously. To identify new interactions with DNA repair pathways, we conducted a computational analysis of gene expression in cervical cancer (CaCx) transcriptomic datasets and identified a frequent upregulation of translesion synthesis (TLS) genes. TLS polymerase genes, particularly the gene for POLη (POLH), did not follow this pattern. Characterization of α-HPV oncogene expressing cell lines and premalignant cervical tissue confirm these data. They also show that the increased TLS protein abundance come in response to nucleoside depletion. Primary and transformed cell lines to demonstrate that α-HPV E6 blocks POLη induction by degrading p53. Lack of POLη dooms the pathway, preventing it from facilitating tolerance of replication stress. Failed TLS results in replication fork stalling and collapse into deleterious double strand breaks in the DNA (DSBs). Consequently, cellular genome fidelity decreases in a manner consistent with the mutations that accumulate during CaCx progression. Alterations in TLS are determinants for the efficacy of the chemotherapeutics most often used to treat CaCx (cisplatin and carboplatin). Exogenous expression of POLη protected CaCx cells from cisplatin-associated toxicity/damage, effectively stabilizing their genome. TLS polymerase expression is also a prognostic factor in CaCx. Analysis of the cancer genome atlas database (TCGA) shows increased expression of these genes correlated with over a decade shorter median survival.

2020-05-01 | GSE145976 | GEO

Genome-wide profiling of human gene in HPV16E2 protein expressing human keratinocyte

Project description:In the early stage of human papillomavirus (HPV) infection, E2 and E6 proteins are expressed and elicit specific immune response to clear cervical lesion. HPV E6 protein can reduce type I interferon (IFN) including IFN-? that involves in immune evasion and HPV persistence. To evaluate the role of E2 protein in modulation of the expression of cellular genes as well as innate immune associated genes in HPV associated cervical cancer, genome-wide expression profiling of human primary keratinocytes (HPK) harbouring HPV16 E2 and HPV18 E2 was investigated using microarray assay and innate immune associated genes were analyzed. These results indicated that HPV E2s altered cellular gene expression including immune associated genes. Altered cellular signaling pathways in HPK expressing HPV E2s based on KEGG database. The top 10 canonical pathways include metabolic pathway, cytokine-cytokine receptor interaction, pathway in cancer, viral carcinogenesis, protein processing in endoplasmic reticulum, PI3K-AKT signaling pathway, MAPK signaling pathway, leukocyte transendothelial migration, chemokine signaling, and focal adhesion.

2014-01-14 | GSE54008 | GEO

Genome-wide microRNA profiling of HPV-positive self-samples: Promising triage markers for early detection of cervical cancer

Project description:Offering self-sampling for HPV testing improves the effectiveness of current cervical screening programs. Molecular triage markers directly applicable on self-samples are needed to further stratify HPV-positive women at risk of cervical cancer (so-called triage) and to avoid over-referral and overtreatment. MicroRNAs (miRNAs) deregulation has been implicated in the development of cervical cancer, and represents a potential class of triage markers. However, it is unknown whether deregulated miRNA expression is reflected in self-samples. This study is the first to establish genome-wide miRNA profiles in HPV-positive self-samples to identify miRNAs that can predict the presence of CIN3 and cervical cancer in self-samples. Small RNA sequencing (sRNA-Seq) was conducted to determine genome-wide miRNA expression profiles in 73 HPV-positive self-samples of women with and without cervical precancer (CIN3). The optimal miRNA marker panel for CIN3 detection was determined by GRidge, a penalized method on logistic regression. Classification of sRNA-Seq data yielded a panel of 9 miRNAs with a combined Area Under the Curve (AUC) of 0.89 for CIN3 detection. Six out of nine miRNAs were validated by qPCR in 165 independent HPV-positive self-samples and resulted in a combined AUC of 0.72 for CIN3+ detection. This study shows that deregulated miRNA expression associated with CIN3 and cervical cancer development can be detected in HPV-positive self-samples using genome-wide miRNA profiling. Further validation by qPCR indicates that miRNA expression analysis offers a promising novel molecular triage strategy for CIN3 and cervical cancer detection applicable to self-samples.

2018-01-01 | GSE104758 | GEO

Gene Expression Profiles of HPV-Positive and -Negative Head/Neck and Cervical Cancers

Project description:Human papillomaviruses (HPVs) are associated with nearly all cervical cancers (CCs), 20-30% of head and neck cancers (HNCs), and other cancers. Because HNCs also arise in HPV-negative patients, this type of cancer provides unique opportunities to define similarities and differences of HPV-positive versus HPV-negative cancers arising in the same tissue. Here, we describe genome-wide expression profiling of 84 HNCs, CCs and site-matched normal epithelial samples in which we used laser capture microdissection to enrich samples for tumor-derived versus normal epithelial cells. This analysis revealed that HPV+HNCs and CCs differed in their patterns of gene expression yet shared many changes compared to HPV-HNCs. Some of these shared changes were predicted, but many others were not. Notably, HPV+HNCs and CCs were found to be upregulated in their expression of a distinct and larger subset of cell cycle genes than observed in HPV-HNC. Moreover, HPV+ cancers over-expressed testis-specific genes that are normally expressed only in meiotic cells. Many, though not all, of the hallmark differences between HPV+HNC and HPV-HNC were a direct consequence of HPV and in particular the viral E6 and E7 oncogenes. This included a novel association of HPV oncogenes with testes specific gene expression. These findings in primary human tumors provide novel biomarkers for early detection of HPV+ and HPV- cancers, and emphasize the potential value of targeting E6 and E7 function, alone or combined with radiation and/or traditional chemotherapy, in the treatment of HPV+ cancers. Keywords: Gene expression ptofiles of primary cancers

2007-05-15 | GSE6791 | GEO

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