Genome-wide analysis of gene expression regulated by FSCN1 in cervical cancer HeLa cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA628702 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11616300_1.fastq.gz | Fastqsanger.gz | |||
| SRR11616300_2.fastq.gz | Fastqsanger.gz | |||
| SRR11616301_1.fastq.gz | Fastqsanger.gz | |||
| SRR11616301_2.fastq.gz | Fastqsanger.gz | |||
| SRR11616302_1.fastq.gz | Fastqsanger.gz |
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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.
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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.
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Project description:Fascin actin-bundling protein 1 (FSCN1) is an evolutionarily conserved actin-bundling protein that plays a critical role in cell migration, motility, adhesion and cellular interactions. Although multiple clinical studies have implicated the expression of FSCN1 in laryngeal squamous cell carcinoma (LSCC) progression, the precise mechanism of FSCN1 in the process has not been clearly elucidated. To define FSCN1 function, we characterized FSCN1-interacting proteins in LSCC cells by immunoprecipitation followed by LC-MS/MS. After data filtering, 119 proteins with expression in both the Hep-2 and TU-177 cell samples were identified as FSCN1-interacting partners. With in-depth bioinformatics analysis, we linked FSCN1 to critical cellular processes including cell adhesion, glycolysis/gluconeogenesis, regulation of protein ubiquitination, ribosomal RNA processing and small molecule metabolism. We discuss the interactions between FSCN1 and some of the newly validated partners. The identification of these potential partners of FSCN1 expands our knowledge of the FSCN1 interactome and provides a valuable resource for understanding the functions of this protein in LSCC progression.
2019-09-09 | PXD013072 | Pride
Project description:Hyperthermia (HT) is widely used to treat patients with various cancers. In general, HT elicits a wide spectrum of stress responses such as induction of heat shock proteins, protein aggregation and cell death in mammalian cells. Although many biological processes are affected by HT, the overall responses to HT in mammalian cells remain unknown. The effects of heat stress at 41°C for 30 min (mild hyperthermia) on the gene expression in human cervical squamous cell carcinoma HeLa cells were investigated using an Affymetrix GeneChip system.
2013-01-24 | GSE43701 | GEO
Project description:Hyperthermia (HT) is widely used to treat patients with various cancers. In general, HT elicits a wide spectrum of stress responses such as induction of heat shock proteins, protein aggregation and cell death in mammalian cells. Although many biological processes are affected by HT, the overall responses to HT in mammalian cells remain unknown. The effects of heat stress at 41M-BM-0C for 30 min (mild hyperthermia) on the gene expression in human cervical squamous cell carcinoma HeLa cells were investigated using an Affymetrix GeneChip system. Human cervical squamous cell carcinoma HeLa cells were treated with heat stress (41M-BM-0C for 30 min) and followed by incubation for 0, 1, or 3 h at 37M-BM-0C. Non-treated cells were served as control. Total RNA samples were prepared from the cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was monitored by an Affymetrix GeneChipM-BM-. system with a Human Genome U133-plus 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturerM-bM-^@M-^Ys instructions.
2013-01-24 | E-GEOD-43701 | biostudies-arrayexpress
Project description:We aimed to compare the exosomal microRNA profile form HeLa cell line with that from human cervical epithelial cell(Hcer)line.exosomes were isolated from conditioned medium of HeLa cell and HCer cell,3 samples for each group.Exosomal microRNAs were sequenced on Proton Sequencers according to Ion PI Hi-Q Sequencing 200 Kit (Life Technologies).According to the results of miRNA sequencing, we found a total 371 different miRNAs the amount of which reach to 10 fold differece between two groups.
2020-02-26 | GSE128803 | GEO
Project description:Fascin actin-bundling protein 1 (FSCN1), an actin-bundling protein associated with cell migration and invasion, is highly expressed in various tumor tissues. FSCN1 has also been reported to be a marker of increased invasive potential in cervical cancers. However, the functions of FSCN1 are still not fully understood in cervical cancers. Here, the gene expression profile of HeLa cells transfected with FSCN1 shRNA (shFSCN1) was compared with that of cells transfected with empty vector (shCtrl). The results showed that shFSCN1 extensively affected the transcription level of 5,043 genes in HeLa cells. In particular, Gene Ontology (GO) analysis showed that a large number of upregulated genes were annotated with terms including transcription regulation and DNA binding. The downregulated genes were enriched in some cancer pathways, including angiogenesis and cell adhesion. qPCR validation confirmed that FSCN1 knockdown significantly affected the expression of selected genes in HeLa cells either negatively or positively. Expression analysis in TCGA (The Cancer Genome Atlas) revealed that FSCN1 had negative correlations with several transcription factors and a positive correlation with an angiogenic factor (angiopoietin like 4, ANGPTL4) in cervical tumor tissue. In particular, validation by Western blotting showed that FSCN1 knockdown decreased the protein level of ANGPTL4. Our results demonstrated that FSCN1 is not only an actin-binding protein but also a transcriptional regulator and an angiogenic factor in cervical cancer. Thus, our study provides important insights for further study on the regulatory mechanism of FSCN1 in cervical cancer.
| S-EPMC8817631 | biostudies-literature
Project description:Several copy number altered regions (CNA) have been identified in the genome of cervical cancer, especially amplifications of 3q and 5p. However, the contribution of those alterations to cervical carcinogenesis is still a matter of debate, since genome-wide, there is a lack of correlation between CNAs and gene expression. In this study, we investigated whether the CNAs in cell lines (CaLo, CasKi, HeLa, SiHa), at a gene-by-gene level, are related to changes in gene expression. On average 19.2% of the whole genome of cell lines had CNA. However, only 2.4% consisted of minimal recurrent regions (MRR), common to all cell lines. Whereas 3q had just some sparse common gains (13%), 5p was entirely duplicated recurrently. Genome-wide, only 11% of genes located in CNAs changed gene expression. In contrast, the rate increased over 3 fold times in MRRs. Chr 5p was confirmed entirely amplified by FISH. In spite of this, at most 32.9% of the explored genes in 5p (n=202) were de-regulated. In 3q, the rate was just 11.8%. Even in 3q26, which had five MRRs and 38.7% of SNPs was gained recurrently, the rate rose slightly to 13.6% (10 out of 73). Interestingly, up to 16% of de-regulated genes in 5p and 80% in 3q26 were down-regulated, suggesting additional factors are involved in gene repression. The de-regulated genes in 3q and 5p were found in clusters, suggesting local chromatin factors may also influence gene expression. In regions amplified discontinuously, the rate of down-regulated genes rose steadily as the number of amplified SNPs increased (p<0.01, Spearman's correlation). This suggests partial gene amplification as a mechanism of silencing gene expression. Additional genes were identified up- or down-regulated in 5p and 3q, which could be involved in cervical carcinogenesis, especially implicated in apoptosis. Those include CLPTM1L, AHRR, PDCD6 and DAP in 5p and TNFSF10 and ECT2 in 3q. Overall, the gene expression and copy number profiles suggest other factors, like epigenetic or chromatin domains, may influence gene expression within the entirely amplified genome segments. Further studies are needed to elucidate how these mechanisms regulate gene expression. We analyzed four cervical cancer cell lines and normal exocervix tissue from 10 healthy female subjects using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Affymetrix Exon Array Computational Tool. Biological replicates were performed for the cell lines. biological replicate: Calo-a, Calo-b biological replicate: Caski-a, Caski-b biological replicate: Hela-a, Hela-b biological replicate: Siha-a, Siha-b
2011-07-31 | E-GEOD-29216 | biostudies-arrayexpress