Similar Datasets
Project description:We perfomed RNA-seq analysis using HPV16-postive CaSki and SiHa cells and HPV18-postive HeLa cells for HPV integration and gene expression analyses
2022-03-30 | GSE158033 | GEO
Project description:By using HeLa as our model system, which has integration in the most recurrently integrated TAD in the cervical tumors i.e. TAD3189, we show most of the interactions of integrated HPV18 DNA is constrained within the TAD with integration. Similarly, TAD3189 also showed very high and most significant allele specific expression among all the TADs on chr8, in HeLa. The integrated HPV18 DNA also showed strong chromatin looping interactions with the oncogenes present in the TAD3189 which were ~500kb away from the integration. These oncogenes in the TAD3189 further showed high allele specific expression from the haplotype with HPV18 integration, possibly representing the cis-regulatory potential of integrated HPV DNA.
2023-11-18 | GSE247605 | GEO
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
Project description:Human cancer cell lines are the most frequently used preclinical models in the study of cancer biology and the development of therapeutics. Although anatomically diverse, human papillomavirus (HPV)-driven cancers have a common etiology and similar mutations that overlap with but are distinct from those found in HPV-negative cancers. Building on prior studies that have characterized subsets of head and neck squamous cell carcinoma (HNSCC) and cervical squamous cell carcinoma (CESC) cell lines separately, we performed genomic, viral gene expression, and viral integration analyses on 74 cell lines that include all readily-available HPV-positive (9 HNSCC, 8 CESC) and CESC (8 HPV-positive, 2 HPV-negative) cell lines and 55 HPV-negative HNSCC cell lines. We used over 700 human tumors for comparison. Mutation patterns in the cell lines were similar to those of human tumors. We confirmed HPV viral protein and mRNA expression in the HPV-positive cell lines. We found HPV types in three CESC cell lines that are distinct from those previously reported. We found that cell lines and tumors had similar patterns of viral gene expression; there were few sites of recurrent HPV integration. As seen in tumors, HPV integration did appear to alter host gene expression in cell lines. The HPV-positive cell lines had higher levels of p16 and lower levels of Rb protein expression than did the HPV-negative lines. Although the number of HPV-positive cell lines is limited, our results suggest that these cell lines represent suitable models for studying HNSCC and CESC, both of which are common and lethal.
2018-11-15 | GSE122512 | GEO
Project description:Human papillomaviruses (HPVs) cause most cervical cancers and an increasing number of other anogenital and oral carcinomas, with most cases caused by HPV16 or HPV18. HPV hijacks host signalling pathways to promote proliferation, to drive carcinogenesis. Understanding these interactions could permit identification of much-needed therapeutics for HPV-driven malignancies. The Hippo signalling pathway is important in HPV+ cancers, with the downstream effector YAP playing a pro-oncogenic role. However, the significance of its paralogue TAZ remains largely uncharacterised in these cancers. We demonstrate that TAZ is dysregulated in a HPV-type dependent manner by a distinct mechanism to that of YAP and controls proliferation via alternative cellular targets. Analysis of cervical cancer cell lines and patient biopsies revealed that TAZ expression was only significantly increased in HPV18+ and HPV18-like cells and. TAZ knockdown reduced proliferation, migration, and invasion only in HPV18+ cells. RNA-sequencing of HPV18+ cervical cells revealed that YAP and TAZ have distinct targets, suggesting they promote different mechanisms. Thus, in HPV18+ cancers, YAP and TAZ play non-redundant roles. This analysis identified TOGARAM2 as a previously uncharacterised TAZ target and demonstrates its role as a key effector of TAZ-mediated proliferation, migration, and invasion in HPV18+ cancers.
2024-05-20 | GSE261673 | GEO
Project description:We perfomed Targeted DNA-seq analysis using MmuPV1 infected mouse warts and uninfected control tissues for MmuPV1 integration analyses
2021-07-14 | GSE163681 | GEO
Project description:We perfomed RNA-seq analysis using MmuPV1 infected mouse warts and control tissues for MmuPV1 integration and host gene expression analyses
2021-07-14 | GSE163537 | GEO
Project description:Identification of genes differentially expressed in tumorigenic compared to non-tumorigenic, HPV18 positive cells Keywords: ordered We used microarrays to identify genes differentially expressed in tumorigenic HeLa x fibroblast hybrid cells (CGL3) and parental HeLa cells compared to non-tumorigenic HeLa x fibroblast hybrid cells (444). Gene expression profiles of proliferating cells under cell culture conditions were compared to identify differential gene expression patterns of upregulated and downregulated mRNA expression patterns of tumorigenic CGL3 and HeLa cells versus non-tumorigenic 444 cells..
2013-11-27 | E-GEOD-14052 | biostudies-arrayexpress
Project description:Infection with oncogenic human papillomavirus (HPV) is a major cause for the development of cervical cancer, which is mainly driven by the expression of the HPV E6 and E7 oncoproteins. We uncovered that the concentration levels of the putative tumor suppressor Dickkopf-1 (Dkk1) are restricted in cervical cancer cells by HPV E6 expression due to the E6-mediated proteolytic degradation of p53, which is a transcriptional regulator of Dkk1. Moreover, we found that Dkk1 is critically involved in the pro-apoptotic Cisplatin response of these cells, as Dkk1 repression was associated with an increased resistance towards the chemotherapeutic compound. This could be of high relevance for cervical cancer treatments, which usually involve Cisplatin for standard care. Although Dkk1 is a major antagonist of the canonical Wnt signaling, the differential response towards Cisplatin observed in Dkk1-depleted cells was not associated to an activation of this pathway. To elucidate alternative underlying mechanisms, we performed Affymetrix Gene Expression analyses comparing the transcriptome of Cisplatin-treated parental HeLa to CRISPR/Cas9-generated Dkk1 knockout (KO) HeLa cells. These revealed that Dkk1 depletion is linked to an impairment of the pro-apoptotic JNK/AP-1 pathway in cervical cancer cells, suggesting that Dkk1 drives Cisplatin-mediated apoptosis via activation of this signaling hub.
2022-08-16 | GSE200748 | GEO
Project description:To further explore the expression profile of lncRNAs and mRNAs in cervical cancer, six cases of HPV-positive cervical cancer tissues (including three HPV16 and three HPV18 positive patients) and three HPV-negative normal cervical tissues were collected randomly that were confirmed by histopathological. These patients did not accept any local or systemic treatment.
2023-05-25 | GSE228568 | GEO