PNAs-A15 effects on cervical cancer cells line
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE76258 | GEO | 2015/12/23
SECONDARY ACCESSION(S): PRJNA306743
REPOSITORIES: GEO
Similar Datasets
Project description:Expression profile of HeLa and C33A cervical cancer cells line treated with PNAs-A15 for 6 hours. PNAs-A15 is peptide nucleic acid of A-repeats length 15 bp that can suppress up-regulated A-repeats containing genes in cervical cancer cells line. The cervical cancer cell line HeLa and C33A was maintained at 37C in 5% CO2 under sterile conditions in Dulbecco's modified Eagle medium, supplemented with 10% fetal bovine serum. Cells were treated with PNAs-A15 in 6-well microplates for 6 h. Total RNA was isolated and hybridized on the HumanHT-12 v4 Expression BeadChip. The RNA expressions were evaluated and compared with 2 repeats of controlled experiments.
2015-12-23 | E-GEOD-76258 | biostudies-arrayexpress
Project description:Expression profile of parental wild type non-small cell lung cancer, NCI-H460, and cancer stem cell-rich (CSC-rich) populations treated with PNAs-A15 for 6 h. Results provide the information that PNAs-A15, a peptide nucleic acid of A-repeats length 15 bp, suppressed up-regulated A-repeats containing genes in both parental wild type and CSC-rich cells.
2016-03-17 | GSE79308 | GEO
Project description:Expression profile of parental wild type non-small cell lung cancer, NCI-H460, and cancer stem cell-rich (CSC-rich) populations treated with PNAs-A15 for 6 h. Results provide the information that PNAs-A15, a peptide nucleic acid of A-repeats length 15 bp, suppressed up-regulated A-repeats containing genes in both parental wild type and CSC-rich cells. In this study, we isolate cancer stem cell-rich (CSC-rich) population from a non-small cell lung cancer (NSCLC) cell line, NCI-H460, by selectively propagating the cells in a spheroid culture condition. The parental wild type H460 and CSC-rich cells were maintained at 37°C in 5% CO2 under sterile conditions in Roswell Park Memorial Institute (RPMI) 1640 medium. Cells were treated with PNAs-A15 in 6-well microplates for 6 h. Total RNA was isolated and hybridized on the HumanHT-12 v4 Expression BeadChip. The RNA expressions were evaluated.
2016-03-17 | E-GEOD-79308 | biostudies-arrayexpress
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:Prior investigations have delineated the multifarious roles of EGFL7 within various cancer contexts. Nevertheless, the precise involvement of EGFL7 in the realm of human cervical carcinoma remains unclear. In this study, we investigated the relationship between EGFL7 polymorphisms and cervical cancer susceptibility in the Han Chinese population. Concurrently, we have scrutinized the expression patterns of EGFL7 in both the neoplastic cervical tissues and the cell lines HeLa and C33A. Furthermore, we explored the potential biological functions that EGFL7 may assume in the tumorigenesis of cervical cancer. Our findings manifest that the single nucleotide polymorphism rs9411260, ensconced within the transcriptional regulatory domain of EGFL7, is associated with cervical cancer risk in a Han Chinese population. Additionally, the mRNA expression of EGFL7 within cervical carcinoma tissues and the HeLa and C33A cell lines exhibits a marked reduction when compared with their adjacent normal counterparts and ECT1/E6E7 cells. Manipulation of EGFL7 expression precipitates alterations in the adhesion and migratory ability of cervical cancer cells. This investigation endows us with novel insights into the pathogenesis of cervical cancer.
2023-12-31 | GSE248647 | GEO
Project description:Four cervical carcinoma cell lines (C4I, CaSki, HeLa, SiHa) were treated with epigenetic modifying drugs 5-aza-2’-deoxycytidine and trichostatin A. Such treatment leads to reactivation of genes that are epigenetically silenced in cancer by aberrant methylation; reactivated genes were then identified by microarray profiling. Subsets consist of 2 biological repeats and 2 dye-flip experiments for each repeat for CaSki cell line, and 3 repeats, each with 2 dye-flip experiments for C4I, HeLa, Caski cell lines. The identification of reactivated genes, their selection for validation experiments, and final identification of 6 genes that are significantly more often hypermethylated in cervical carcinoma clinical specimens is described in (manuscript submitted). Keywords: other
2005-07-17 | GSE2097 | GEO
Project description:Five human cervical cancer cell lines (HeLa, CaSki, SiHa, C-33A, SW756) and one human normal cervical epithelial cell line HcerEpic were included in the study. Microarray based circRNA expression profiles were acquired using the Arraystar Human circRNA Array (8x15K, Arraystar). We identified circRNAs differentially expressed in human cervical cancer cell lines compared to human normal cervical epithelial HcerEpic cells (control).
2018-04-27 | GSE113696 | GEO
Project description:This analysis aimed to identify differentially expressed genes in Cervical Cancer derived cell lines. The working cell lines were SiHa, HeLa and C33A. The non-tumorigenic HaCaT cell line was included as control. mRNA sequencing was performed on the Illumina NovaSeq 6000 platform by Novogene Bioinformatics Technology Co., Ltd, Beijing, China, with two independent replicate sequences for each cell model. Methodology: The execution of the bioinformatics pipeline analysis was carried out according to the following description: Rstudio (v2023.06.1+524) and Galaxy (https://www.usegalaxy.orgaccessed on 15 August 2023) open-source platforms were used to analyze the Illumina raw data. The Quality Check was conducted through the FastQC tool (v0.12.1). Afterward, all the reads were processed by the Rsubread package (v2.14.2); at that point, the reads were trimmed and aligned to the Human Genome Reference (GRCh38.p14 v43). The obtained output was: the BAM files, of which the number of reads was counted by the featureCounts tool (v2.0.3); at the final step, the Differential Expression Analysis was settled by the DESeq2 tool (v2.11.40.8). The differential gene expression measurements were normalized by DESeq2's median of ratios (median of ratio of gene counts relative to geometric mean per gene) method. All chemokine genes with an adjusted p-value (adj p) minus or equal to 0.05 and fold change (Log2FC) up to 2 or less than minus 2 were selected as differentially expressed genes (DEGs). Some genes from the resulting outputs were validated through qPCR. Conclusions: Our study found 5850 differentially expressed genes for SiHa cell lines, 6698 for HeLa, and 6707 for C33a.
2023-11-02 | GSE241703 | GEO
Project description:Cervical cancer stands as one of the leading causes of cancer-related mortality in women worldwide, yet the precise functions of host genes implicated in its pathogenesis remain elusive. Genome-wide association studies (GWAS) have revealed a significant association between the CLPTM1L locus and cervical cancer risk in European women, and aberrant expression of CLPTM1L has been noted in various malignant tumors. However, the role of CLPTM1L in cervical cancer remains largely unexplored. This study aimed to explore the biological function of CLPTM1L in cervical cancer. The expression of CLPTM1L in cervical cancer cells and tissues was detected by RT-qPCR. Furthermore, the potential biological functions of CLPTM1L in the context of cervical cancer were explored via RNA sequencing. Cell proliferation rates and the responsiveness of cervical cancer cells to cisplatin were evaluated using the CCK-8 assay, while cell apoptosis was quantified through the utilization of flow cytometry. Nude mouse xenograft models were utilized to explore the impact of CLPTM1L on tumor formation in vivo. Our findings demonstrated a significant increase in CLPTM1L mRNA expression levels in HeLa and C33A cells, as well as in cervical carcinoma tissues, compared to ECT1/E6E7 cells and adjacent normal tissues. Genes related to CLPTM1L were found to be enriched in the Hedgehog signaling pathway. In vitro and in vivo studies showed that reducing CLPTM1L expression markedly inhibited cell proliferation via downstream candidate genes BOC and LRP2. Furthermore, the downregulation of CLPTM1L was found to enhance cisplatin-induced cell apoptosis and increase the susceptibility of cervical cancer cells to cisplatin through DAP1. This investigation has bestowed upon us novel insights into the pathogenesis of cervical cancer, underscoring the potential of CLPTM1L as a promising target for chemotherapeutic sensitization in the management of this malignancy.
2024-08-31 | GSE267713 | GEO