ChIP-Seq hnRNP E1, Cervical cancer SiHa cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE203023 | GEO | 2022/06/16
REPOSITORIES: GEO
Similar Datasets
Project description:ChIP-Seq hnRNP E1, Cervical cancer SiHa cells
| PRJNA838137 | ENA
Project description:This study assessed the transcriptional profile of SiHa cells. SiHa is a cervical cancer cell line with integrated HPV16, and was used as a model to study human gene expression in the context of integrated virus. Gene expression in SiHa, calculated by Cufflinks, was scored in windows around the locations of known viral integrations in patients or cell lines to determine if there was an association between gene expression and viral integration. We found that SiHa gene expression was higher near loci of integration for HPV18 vs. HPV16, cervical tissues vs. head and neck cancers, and cervical cancers vs. in vitro integrations. This study provides insight into the factors that may influence where viruses integrate in the human genome.
2015-11-30 | GSE67115 | GEO
Project description:circCDKN2B-AS1 is significantly upregulated circRNA in HPV16 positive cervical cancer tissues comprared with both HPV16 positive and HPV16 negative normal cervical tissues.So we chose it for further study.To explore the mRNA expression profiles following circCDKN2B-AS1 knockdown, we performed RNA sequencing analysis in SiHa cells with or without circCDKN2B-AS1 knockdown.We performed RNA sequencing in two pairs of RNA samples of SiHa cells with or without circCDKN2B-AS1 knockdown.
2020-12-21 | GSE147010 | GEO
Project description:To investigate the different gens expression in the cervical immortalized cervical cells (H8 cells), cervical cancer cells (SiHa cells) and KD HSPA9 SiHa cells.
2023-06-25 | GSE235550 | GEO
Project description:Regulation of gene expression at the post-transcriptional level plays an indispensable role during TGFbeta-induced EMT and metastasis. This regulation involves a transcript-selective translational regulatory pathway in which a ribonucleoprotein (mRNP) complex, consisting of heterogeneous nuclear ribonucleoprotein E1 (hnRNP E1) and eukaryotic elongation factor 1A1 (eEF1A1), binds to a 3M-bM-^@M-^Y-UTR regulatory BAT (TGFM-NM-2 activated translation) element and silences translation of Dab2 and ILEI mRNAs, two transcripts which are involved in mediating EMT. TGFbeta activates a kinase cascade terminating in the phosphorylation of hnRNP E1, by isoform-specific stimulation of protein kinase B/Akt2, inducing the release of the mRNP complex from the 3M-bM-^@M-^Y-UTR element, resulting in the reversal of translational silencing and increased expression of Dab2 and ILEI transcripts. We adopted a combinatorial approach involving polysome profiling and RIP-Chip analyses using hnRNP E1 and filtered the array data based on the regulatory mechanism of Dab2 and ILEI. This led to the identification and validation of a cohort of target mRNAs that follow the same pattern of regulation as Dab2 and ILEI. To identify potential target mRNA transcripts that are translationally regulated by hnRNP E1 in a TGF-beta-dependent manner, we adopted a combinatorial approach involving expression profiling analyses and RNA immunoprecipitation analysis (RIP-Chip). We performed a screen using: 1) total mRNA and 2) RNA isolated from monosomal (non-translating) versus polysomal (translating) fractions from TGF-beta-treated (24 h) and non-treated NMuMG cells and from the hnRNP E1 knockdown derivative (E1KD), that undergo constitutive EMT even in the absence of TGF-beta. In addition, we screened for transcripts that selectively interact with hnRNP E1 in NMuMG cells under unstimulated conditions and subsequently lose their temporal association following TGF-beta stimulation. The samples were individually hybridized to Affymetrix GeneChipM-BM-. Mouse Genome 430 2.0 arrays.
2012-08-30 | E-GEOD-40466 | biostudies-arrayexpress
Project description:Regulation of gene expression at the post-transcriptional level plays an indispensable role during TGFbeta-induced EMT and metastasis. This regulation involves a transcript-selective translational regulatory pathway in which a ribonucleoprotein (mRNP) complex, consisting of heterogeneous nuclear ribonucleoprotein E1 (hnRNP E1) and eukaryotic elongation factor 1A1 (eEF1A1), binds to a 3’-UTR regulatory BAT (TGFβ activated translation) element and silences translation of Dab2 and ILEI mRNAs, two transcripts which are involved in mediating EMT. TGFbeta activates a kinase cascade terminating in the phosphorylation of hnRNP E1, by isoform-specific stimulation of protein kinase B/Akt2, inducing the release of the mRNP complex from the 3’-UTR element, resulting in the reversal of translational silencing and increased expression of Dab2 and ILEI transcripts. We adopted a combinatorial approach involving polysome profiling and RIP-Chip analyses using hnRNP E1 and filtered the array data based on the regulatory mechanism of Dab2 and ILEI. This led to the identification and validation of a cohort of target mRNAs that follow the same pattern of regulation as Dab2 and ILEI.
2012-08-30 | GSE40466 | GEO
Project description:To further identify the most significantly changed miRNA resulting from the different expression levels of TWIST2 in cervical cancer cells, we used a miRNA microarray to identify the miRNA expression profiles among SiHa, SiHa-tw2 and SiHa-shtw2. The significantly deregulated miRNAs (changes of more than 2-fold in expression) included miR-23b-5p, miR-221-3p, miR-502-3p, miR-221-5p, miR-15a-5p, miR-1227, miR-93-5p and miR-4257.
2017-11-21 | GSE102706 | GEO
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:The Kaposi sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi sarcoma (KS), the most common HIV/AIDS-associated tumor worldwide. Transmission routes of KSHV in the general population are poorly understood. Whereas sexual transmission appears to be common in homosexual men, the evidence for heterosexual transmission is less convincing. In fact, KSHVDNA sequences have been detected in the prostate, semen, and in the female genital tract. Persistent infection with high-risk human papillomavirus (HPV) is the major risk factor and is a requirement for the development of cervical cancer. However, it remains unknown the interaction between KSHV and HPV, and the contribution of KSHV to cervical cancer development and pathogenesis. In the present study, we used Illumina microarray to detect the global gene profile altered in KSHV-infected siHa cervical cancer cell-line containing integrated HPV16 genome.
2017-08-13 | GSE90039 | GEO
Project description:Aim was to identify cellular factors that regulate HPV-16 late gene expression at the level of RNA processing Cervical cancer cells permissive for HPV16 late gene expression were identified and characterized. These cells either contained a novel spliced variant of the L1 mRNAs that bypassed the suppressed HPV16 late, 5’-splice site SD3632, produced elevated levels of RNA-binding proteins SRSF1 (ASF/SF2), SRSF9 (SRp30c) and HuR that are known to regulate HPV16 late gene expression, or were shown by a gene expression array analysis to overexpress the RALYL RNA-binding protein of the hnRNP C-family. Overexpression of RALYL, or RALY and hnRNP C1 that are two other members of the hnRNP C-family, induced HPV16 late gene expression from HPV16 subgenomic plasmids and from episomal forms of the full-length HPV16 genome. Induction of HPV16 late gene expression by the hnRNP C-proteins was dependent on the HPV16 early untranslated region to which these proteins also were shown to bind in vitro, and in living cells. Our experiments revealed that hnRNP C proteins that interacted with the HPV16 early untranslated region reached out to the splicing silencer complex at HPV16 SD3632 and derepressed this splice site, thereby activating production of HPV16 spliced late L1 mRNAs. In conclusion, hnRNP C- proteins bind to the HPV16 early untranslated region and control of HPV16 late L1 mRNA splicing.
2015-06-12 | GSE65166 | GEO