Ontology highlight
ABSTRACT:
PROVIDER: PRJNA903697 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22393800_1.fastq.gz | Fastqsanger.gz | |||
| SRR22393800_2.fastq.gz | Fastqsanger.gz | |||
| SRR22393801_1.fastq.gz | Fastqsanger.gz | |||
| SRR22393801_2.fastq.gz | Fastqsanger.gz | |||
| SRR22393802_1.fastq.gz | Fastqsanger.gz |
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Project description:Certain types of Human papilloma viruses (HPV) are the etiological agents for cervical cancer. However, not all infections of high-risk HPVs will finally lead to cancer since most HPV infections are cleared without any consequences. Chlamydia trachomatis is the most prevalent sexual transmitted bacteria and is an obligatory intracellular pathogen exhibiting tropism in endocervical epithelial cells. Over the past decades, C. trachomatis is thought to be a potential co-factor for cervical cancer formation, but there are also studies that did not show such a correlation. To address this question in molecular terms, we stably expressed HPV16 E6 and E7 in spontaneously immortalized NOKs (normal oral keratinocytes) and performed SILAC (stable isotope labeling by amino acids in cell culture) with or without C. trachomatis infection to study the impact of HPV16 oncogene expression and C. trachomatis infection on host proteome changes.
2019-03-18 | PXD012186 | Pride
Project description:Chlamydia trachomatis is an obligate intracellular Gram-negative bacterium that frequently causes an asymptomatic genital tract infection, gradually cleared by host immunity Transcriptome profiles were made of endometrial tissue from women with or without genital tract C. trachomatis infection, to characterize host responses to infection. Profiles showed that infection polarized host defense toward Type 2 immune responses. Responses included fibrin deposition, enhanced wound repair, and tissue remodeling. Trans-cervical endometrial biopsy specimens were collected from 10 women with no identified upper or lower genital tract infection and 12 women with C. trachomatis endometrial infection.
2013-03-01 | E-GEOD-41075 | biostudies-arrayexpress
Project description:Coinfections with pathogenic microbes continually confront cervical mucosa, yet their implications in pathogenesis remain unclear. Lack of in-vitro models recapitulating cervical epithelium has been a bottleneck to study coinfections. Using patient-derived ectocervical organoids, we systematically modelled individual and coinfection dynamics of Human papillomavirus (HPV)16 E6E7 and Chlamydia, associated with carcinogenesis. The ectocervical stem cells were genetically manipulated to introduce E6E7 oncogenes to mimic HPV16 integration. Organoids from these stem cells develop the characteristics of precancerous lesions while retaining the self-renew capacity and organize into mature stratified epithelium similar to healthy organoids. HPV16 E6E7 interferes with Chlamydia development and induces persistence. Unique transcriptional and post-translational responses induced by Chlamydia and HPV lead to distinct reprogramming of host cell processes. Strikingly, Chlamydia impedes HPV-induced mechanisms that maintain cellular and genome integrity, including mismatch repair in the stem cells. Together, our study employing organoids demonstrate the hazard of multiple infections and the unique cellular microenvironment they create, potentially contributing to neoplastic progression.
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Project description:Chlamydia trachomatis are the etiological agents of a range of diseases and are epidemiologically associated with cervical and ovarian cancers. The interplay between host and chlamydia is highly complex, and to obtain panoramic view of the functional interplay, we performed combinatorial global phosphoproteomic and transcriptomic analyses of C. trachomatis-induced signaling. We identified numerous previously unknown C. trachomatis phosphoproteins and C. trachomatis-regulated host phosphoproteins that are substrates of kinases involved in various cellular processes. Interestingly, several host transcription factors (TFs) that are phosphorylated in C. trachomatis infections, including ETS2 repressor factor (ERF), proto-oncogenic transcription factor ETS1 are targets of ERK MAPK signaling. While these TFs were found to be essential for Chlamydia development, we demonstrated their involvement in inducing epithelial-to-mesenchymal transition in C. trachomatis infected cells by transcriptional regulation of genes involved in cellular motility and invasion. Our data reveals substantially unexplored complexity of C. trachomatis-induced signaling and provides broader insights into pro-carcinogenic potential of C. trachomatis.
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Project description:Cervical cancer is the second most common malignancy in women worldwide, with high risk subtypes of human papillomavirus (HPV) constituting the major etiological agent. However, only a small percentage of women infected by the virus develop disease suggesting that additional host genetic alterations are necessary for disease progression. In this study we examined the genomes of a panel of commonly used model cervical cancer cell lines using a recently developed whole genome tiling path array for CGH analysis. Detailed analysis of genomic profiles enabled the detection of many novel aberrations which may have been missed by conventional cytogenetic methods. In total, 27 minimal regions of recurrent copy number alteration were identified that are potentially involved in tumorigenesis. Interestingly, fine mapping of the 3q gain, which is associated with the progression of precursor lesions to invasive cervical cancer, identified a minimal region of alteration harboring genes distinct from previous candidates. Novel regions of gene amplification, including the co-amplification of both the Birc and MMP gene clusters on 11q22, were also evident. Lastly, characterization of genomic structure at sites of HPV integration identified the copy number gain of host cellular sequences between the viral-host genomic boundaries in both SiHa and SW756, suggesting a direct role for HPV integration in the development of genetic abnormalities that initiate cervical cancer. This work represents the highest resolution look at a cervical cancer genome to date and offers definitive characterization of the alteration status of these cancer genomes. Keywords: array CGH, copy number, cervical cancer, genetic alterations, HPV integration, 3q
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Project description:Women persistently infected with human papillomavirus (HPV) type 16 are at high risk for development of cervical intraepithelial neoplasia grade 3 or cervical cancer (CIN3+). We aimed to identify biomarkers for progression to CIN3+ in women with persistent HPV16 infection. In this prospective study, 11,088 women aged 20â29 years were enrolled during 1991-1993, and re-invited for a second visit two years later. Cervical cytology samples obtained at both visits were tested for HPV DNA by Hybrid Capture 2 (HC2), and HC2-positive samples were genotyped by INNO-LiPA. The cohort was followed for up to 19 years via a national pathology register. To identify markers for progression to CIN3+, we performed microarray analysis on RNA extracted from cervical swabs of 30 women with persistent HPV16-infection and 11 HPV-negative women. After further validation, we found that high mRNA expression levels of TMEM45A, SERPINB5 and p16INK4a were associated with increased risk of CIN3+ in persistently HPV16-infected women. We aimed at identifying genes differentially expressed in women with persistent HPV16 infection that either progressed to CIN3+ or not. As a test of principle we first compared HPV16 persistently infected women with HPV-negative women.
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Project description:Cervical cancer is the second most common malignancy in women worldwide, with high risk subtypes of human papillomavirus (HPV) constituting the major etiological agent. However, only a small percentage of women infected by the virus develop disease suggesting that additional host genetic alterations are necessary for disease progression. In this study we examined the genomes of a panel of commonly used model cervical cancer cell lines using a recently developed whole genome tiling path array for CGH analysis. Detailed analysis of genomic profiles enabled the detection of many novel aberrations which may have been missed by conventional cytogenetic methods. In total, 27 minimal regions of recurrent copy number alteration were identified that are potentially involved in tumorigenesis. Interestingly, fine mapping of the 3q gain, which is associated with the progression of precursor lesions to invasive cervical cancer, identified a minimal region of alteration harboring genes distinct from previous candidates. Novel regions of gene amplification, including the co-amplification of both the Birc and MMP gene clusters on 11q22, were also evident. Lastly, characterization of genomic structure at sites of HPV integration identified the copy number gain of host cellular sequences between the viral-host genomic boundaries in both SiHa and SW756, suggesting a direct role for HPV integration in the development of genetic abnormalities that initiate cervical cancer. This work represents the highest resolution look at a cervical cancer genome to date and offers definitive characterization of the alteration status of these cancer genomes. Whole genome tiling path array CGH profiles of 8 Cervical Cancer Cell Lines
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Project description:Human papillomavirus (HPV) infection related malignancy remains a severe public health problem worldwide, although HPV prophylactic vaccine has been introduced 15 years ago . HPV-associated cancers comprise 29.1% of all 2.2 million infection-related cancers, including nearly 100% of cervical cancers1 and some head and neck cancers . Cervical cancers are the 3rd most common cancer in women worldwide, HPV16 and 18 account for about 70% of cervical cancers. Moreover, high-risk HPV infection, especially HPV16 infection, is related to a proportion of head and neck epithelial carcinoma in both developed and undeveloped countries. HPV related cancers are most severe in developing countries where HPV prophylactic vaccination rates are low.In this project, we use iTRAQ8plex-labelling proteomics to comparatively study the protein contents in the tumour tissues of early and late stage cervical cancer patietns.
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