Similar Datasets
Project description:KMT2B，a major H3K4 tri-methyltransferase, contributes to the development of various cancers. However, its role in cervical cancer is unclear. We found that KMT2B is upregulated in cervical cancer tissues, which is significantly associated with poor prognosis.To investigate the underlying mechanism of KMT2B in the progression of cervical cancer, we established stable KMT2B-overexpression HeLa cells.Then we compared the whole genome mRNA expression profile of KMT2B overexpression and control HeLa cells using RNA-seq.
2022-08-03 | GSE209928 | GEO
Project description:Analysis of HeLa cells following depletion of BRCA1 tumor supressor using RNAi against BRCA1. Results provide insight into the molecular mechanisms underlying loss of the BRCA1 function. Six samples (three control samples and three BRCA1 depleted samples) have been analysed. For the control, the samples derived from the HeLa cells treated with RNAi against GFP were used.
2010-06-23 | E-GEOD-22259 | biostudies-arrayexpress
Project description:Analysis of HeLa cells following depletion of BRCA1 tumor supressor using RNAi against BRCA1. Results provide insight into the molecular mechanisms underlying loss of the BRCA1 function.
2010-06-09 | GSE22259 | GEO
Project description:Esrrb is a transcription factor implicated in embryonic stem (ES) cell self-renewal, yet its knockout causes intrauterine lethality due to defects in trophoblast development. Here we show that in trophoblast stem (TS) cells, Esrrb is a downstream target of fibroblast growth factor (Fgf) signalling and is critical to drive TS cell self-renewal. In contrast to its occupancy of pluripotency-associated loci in ES cells, Esrrb sustains the stemness of TS cells by direct binding and regulation of TS cell-specific transcription factors including Elf5 and Eomes. To elucidate the mechanisms whereby Esrrb controls the expression of its targets, we characterized its TS cell-specific interactome by mass spectrometry. Unlike in ES cells, Esrrb interacts in TS cells with the histone demethylase Lsd1 and with the RNA Polymerase II-associated Integrator complex. Our findings provide new insights into both, the general and context-dependent wiring of transcription factor networks in stem cells by master transcription factors.
2015-07-24 | PXD002183 | Pride
Project description:Transcriptional profiling of HeLa cervical carcinoma cells comparing cells with siRNA- or shRNA-mediated depletion of GPRC5A vs. cells carrying non-targeting siRNA or shRNA after 45 min and 6 h of adhesion to 10% Matrigel matrix. The goal was to determine the effect of GPRC5A depeltion on the global gene expression following the adhesion process.
2016-12-31 | GSE68338 | GEO
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:CBL0137 id non-genotoxic DNA binding compounds which directly destabilizes nucleosomes in cells. Effect of different doses of CBL0137 on the abundance of mRNA was studied in two cell types, multiple myeloma MM1.S and cervical carcinoma HeLa cell.
2018-07-25 | GSE117611 | GEO
Project description:BAG3 (BCL2-associated athanogene 3) is a member of the BAG protein family. BAG3 affects a wide variety of cellular events including cell proliferation, apoptosis and autophagy. Recently our data demonstrated that knockout (KO) of BAG3 induces the cell growth arrest in human cervical carcinoma HeLa cells. In the present study, to identify genes involved in the cell growth arrest by BAG3-KO in HeLa cells, global-scale gene expression analysis was carried out using a GeneChip® system.
2017-09-06 | GSE103475 | GEO
Project description:FSCN1 has been reported to be dysregulated in cervical cancers. However, the genome-wide regulated targets of FSCN1 is still unclear in cervical cancers. Here, the gene expression profile of HeLa cells transfected with FSCN1 shRNA (shFSCN1) were compared with cells transfected with empty vector (shCtrl). The results showed that shFSCN1 extensively affects the transcriptional level of 5, 043 genes in HeLa cells. There were more up-regulated genes (3, 870) than down-regulated ones (1, 173) after FSCN1 was knocked down in HeLa cells. GO analysis showed that the up-regulated genes were associated with transcription regulation and DNA binding. The down-regulated genes were enriched in some cancer associated pathway including angiogenesis and cell adhesion. In particular, FSCN1 positilvely regulated ANGPTL4 in HeLa cells. Compared to normal tissue, both FSCN1 and ANGPTL4 showed a higher expression in cervical tumor tissue. Moreover, ANGPTL4 was also positilvely correlated with expression of FSCN1 in cervical tumor tissue of TCGA. In conclusion, our study provide important cues for further study on the regulatory mechanism of FSCN1 in cervical cancer.
2022-01-20 | GSE149450 | GEO
Project description:MicroRNAs (miRNAs) play an important role in the regulation of gene expression and are often dysregulated in disease. The recent development of the CRISPR-Cas9 gene-editing system, composed of the Cas9 nuclease in complex with a single guide RNA (sgRNA), allows researchers to direct DNA cleavage at a predetermined site and to conduct genome-scale knockout screens. To determine the functional role of miRNAs in cancer, we designed and constructed a library of 7,382 sgRNAs to target 85% of the 1,881 annotated human miRNA stem-loops. We then examined the role of miRNAs in HeLa cell fitness by monitoring the change in frequency of each sgRNA over time. We identified 44 pro-proliferative miRNAs from two replicate experiments, including miR-31, a known cervical cancer overexpressing miRNA that enhances HeLa cell proliferation. We also examined the role of miRNAs in NCI-N87 gastric cancer cells and identified 10 pro-fitness and 10 anti-fitness miRNAs. In both screens, many of the pro-fitness miRNAs identified are overexpressed in tumors cervical tumors for HeLa or gastric tumors for NCI-N87. In summary, we present a CRISPR miRNA-targeted screen which was able to identify both known and novel fitness-associated miRNAs in the HeLa and NCI-N87 cell lines.
2018-06-21 | GSE110784 | GEO