Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global gene expression profiled with RNA-Seq in CYH33-resistant ESCC cells as well as their parental cells

ABSTRACT: To investigate the mechanism mediating resistance to CYH33 in ESCC cells, global gene expression was profiled with RNA-Seq in CYH33-resistant cells as well as their parental cells. Gene enrichment analysis revealed that RAS signaling pathway, PI3K-Akt signaling pathway and MAPK signaling pathway were highly activated in most CYH33-resistant cells. To analyze the difference of gene expression profiles between CYH33-resistant cells and their matched parental cells upon CYH33 treatment, cells were treated with CYH33 at 1 μM for 24 hours and RNA-seq was performed. Gene Set Enrichment Analysis was then carried out.

ORGANISM(S): Homo sapiens

PROVIDER: GSE162658 | GEO | 2021/01/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Global gene expression profiled with RNA-Seq in CYH33-resistant ESCC cells as well as their parental cells

Project description:Global gene expression profiled with RNA-Seq in CYH33-resistant ESCC cells as well as their parental cells

| PRJNA682576 | ENA

A chemical screen identifies compounds limiting the toxicity of C9ORF72 dipeptide repeats

Project description:Purpose: Compare parental NSC34 cells with NSC34 PR20-resistant clones Methods: NSC-34 cell cultures were treated with PR20, a peptide that contains 20 copies of Proline-Arginine aminoacids, for two weeks. mRNA profiles of resistant clones were generated by RNAseq. Sequencing reads were aligned and analyzed for differential gene expression. Results: NSC34 clones that gained spontaneous resistance to PR20 present a higher levels of translation than parental cells. Gene Set Enrichment Analysis (GSEA) of this dataset revealed an overall upregulation of factors from the “mTORC1 signaling” hallmark

2021-02-14 | GSE110596 | GEO

In-depth proteomic investigation of isogenic radiation resistant prostate cancer cell lines

Project description:To model radioresistance, we generated radiation resistant cells using conventional (CF) and hypofractionated (HF) treatment schedules. We then evaluated the proteome of CF, HF and parental cells and discovered over 300 dysregulated proteins in the CF and HF cells relative to parental. Pathway analyses revealed upregulation of PI3K AkT mTOR signaling, oxidative phosphorylation, hypoxia, glycolysis, epithelial to mesenchymal transition (EMT), E2F targets and DNA repair in the radioresistant cells. We validated our proteomic findings that CD44 is enriched in CF and HF cells by western blot and flow cytometry. Finally, treatment with blocking anti-CD44 antibody promoted radiosensitization.

2020-12-02 | MSV000086545 | MassIVE

Hypomethylating agents sensitize diffuse large B-cell lymphoma to venetoclax

Project description:We established acquired venetoclax resistant OCI-LY1R cell line by treating venetoclax sensitive parental OCI-Ly1 cell line with increasing doses of venetoclax up till 1µM. Parental OCI-Ly1 and venetoiclax-resistant OCI-Ly1R cells were treated with vehicle control or decitabine at 1uM for 3 days. We found that decitabine differantially regulated gene expression in venetoclax sensitive and resistant cells. With gene set enrichment analysis, we identified two pathways that were deregulated by decitabine in both cell lines.

2023-07-25 | GSE223598 | GEO

CDCA7 promotes TGF-β-induced epithelial-mesenchymal transition via transcriptionally regulating Smad4/Smad7 in ESCC

Project description:Purpose：Cell division cycle associated 7 (CDCA7) is a copy number amplification gene that contributes to the metastasis and invasion of tumors, including esophageal squamous cell carcinoma (ESCC). This present study aimed at clarifying whether high expression of CDCA7 promotes the metastasis and invasion of ESCC cell lines and exploring the underlying mechanisms implicated in EMT of ESCC. Mehtod：We established KYSE150 cell lines in which target gene has been knocked down by shRNA and KYSE180 cell lines in which target gene has been ovexpressed by plasmid.We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells.Each cell has three repetions. Result：KEGG pathway enrichment analysis on the data of RNA-seq showed that Wnt signaling pathway and TGF-β signaling pathway which are related to EMT process were screened out. Conclusion：CDCA7 was heavily involved in EMT by regulating the expression of Smad4 and Smad7 in TGF-β signaling pathway.

2023-01-11 | GSE201735 | GEO

Transcriptome and phosphoproteome analyses of gemcitabine-resistant gallbladder cancer cells provide novel insights into molecular changes occurring during acquired resistance

Project description:Treatment options for advanced gallbladder cancer (GBC) are scarce and usually rely on cytotoxic chemotherapy, but unfortunately the effectiveness of any regimen is limited, and recurrence rates are high. Here, we established and characterized two gemcitabine-resistant GBC cell sublines (NOZ GemR and TGBC1 GemR) to investigate the molecular mechanisms associated with acquired resistance in vitro. The transcriptome profiling of parental and gemcitabine resistant cells revealed differential expression of multiple protein-coding genes and enrichment of biological processes such as epithelial-to-mesenchymal transition and drug metabolism. On the other hand, quantitative phosphotyrosine proteomic analysis of NOZ GemR identified aberrantly dysregulated signaling pathways in resistant cells as well as active kinases, such as Abl, PDGFRA, EphB2 and members of the Src-family that could be novel therapeutic targets against drug resistance in GBC. In line with this, NOZ GemR cells showed increased sensitivity toward the multikinase inhibitor dasatinib compared with parental cells. In conclusion, our study describes transcriptome changes and altered signaling pathways occurring in gemcitabine-resistant gallbladder cancer cells, which greatly expands our understanding of the underlying mechanisms of acquired drug-resistance in GBC. Moreover, this new gemcitabine resistant GBC models could be exploited either to study alternative mechanisms of resistance or to explore new therapies for chemotherapy-refractory GBC.

2023-05-03 | PXD036348 | Pride

Expression data from the rituximab-resistant lymphoma cell lines and the parental cell lines

Project description:Rituximab, a monoclonal antibody against CD20, has achieved great success in the treatment of B cell lymphoma, but many patients have shown resistance to it and led to disease progression eventually. At present, the mechanism of resistance is still not clear, but we consider that it may involve the multiple genes and multiple signaling pathways. Therefore, our study aimed at searching differentially expressed genes of rituximab resistant cell lines (RRCL) by cDNA microarray, and exploring the resistant mechanism of RRCL by using the subsequent bioinformatics methods. In this study, we successfully identified seventy up-regulated genes and forty-two down-regulated genes in both two RRCL. We also isolated the MAPK signaling pathway, which was the significantly enriched pathway in resistant mechanism, through KEGG pathway analysis. Moreover, we discovered the biological behaviors of RRCL that mainly inhibit apoptosis, promote cellular proliferation, transcription and angiogenesis through Gene Ontology (GO) terms analysis. In conclusion, our results suggested that the most closely related pathway to rituximab resistance was MAPK signaling pathway, which may partly be related to its inhibiting the apoptosis of cells and promoting the proliferation of cells and vascular development. We utilized human mantle cell lymphoma cell line Jeko-1 and human Burkitt lymphoma cell line Raji to establish rituximab resistant Jeko-1/R and Raji/R cell lines. And then, in order to explore rituximab resistant mechanism, we looked for the different gene expression profile of rituximab resistant cell lines compared with the parental cell lines by cDNA microarray and carried out subsequent KEGG pathway and GO terms analysis.

2014-08-13 | E-GEOD-60327 | biostudies-arrayexpress

A randomized, controlled, multicenter, phase I/II study of cetuximab plus irinotecan investigating the pharmacodynamics, genomics and -genetics as well as the safety and efficacy of a dose escalation schedule of cetuximab compared with the standard fixed dosing regimen in patients with irinotecan-resistant EGFR expressing metastatic colorectal cancer.

Project description:Primary objectives: To compare in skin biopsies the effects of an cetuximab dose escalation regimen on EGFR and downstream signaling pathway markers with those of the standard cetuximab regimen Primary endpoints: Expression of EGFR and markers for the downstream signalling pathways in normal skin expressed by means of percentage of stained cells and staining intensity. IHC staining will allow a semi quantitative analysis of protein markers of the EGFR related signalling pathway.

| 2515542 | ecrin-mdr-crc

Activation of Wnt signaling promotes olaparib resistant ovarian cancer.

Project description:Sequencing of olaparib-resistant PEO1 derivatives (C4, C5, C10 and C18) and parental PEO1 (P1 and P2) cells was performed in order to determine mechanisms of acquired resistance in the resistant cell lines. PEO1 parental cell lines were authenticated prior to sequencing. PEO1 parental were confirmed to be BRCA2-mutated (5139C>G). Olaparib PEO1 resistant cells were generated through a step-wise escalation of olaparib (10nM to 8uM olaparib). In olaparib resistant lines an increase canonical Wnt signaling and loss of of non-canonical Wnt signaling was observed.

2018-07-28 | GSE117765 | GEO

Expression Patterns of SOX10 deficient BRAFi/MEKi tolerant and SOX10 KO A375 cell lines

Project description:Given the heterogeneous expression of SOX10 in naïve melanoma, we sought to characterize SOX10 deficient population. To this end, we generated SOX10 CRISPR/Cas9 knockouts using two different guide RNAs (gRNA, #2 and #4) in the A375 (BRAF mutant) metastatic cell line. Using this approach, we identified multiple clones with loss of SOX10 expression. RNA-seq was performed to characterize the SOX10-regulated transcriptome. We used GSEA analysis to evaluate significant pathway changes in SOX10 knockout cells when compared to parental cells. We observed an enrichment in pathways associated with the tumor microenvironment (epithelial-mesenchymal transition; TGF beta signaling; extracellular structure organization; apical junction; hypoxia; angiogenesis), alterations in metabolic pathways (increase in the glycolysis pathway), a reduction in MYC and E2F targets and upregulation in p53 pathway and TNFA signaling via NFkB in the SOX10 knockout cells compared to parental cells. SOX10 negative clones have been identified in the minimal residual disease in BRAF mutant PDX models following BRAF and MEK inhibition and in patient samples while on treatment and SOX10 loss has been described as a resistant mechanism in BRAF mutant melanoma patients following vemurafenib treatment. Thus, we also analyzed the transcriptome profile of SOX10 low/deficient cells that arose following BRAFi+MEKi treatment in vivo. We performed GSEA analysis on RNA-seq data of CRT34 and CRT35 cells compared to parental A375 cells. CRT34 and CRT35 showed a very similar transcriptome profile to SOX10 KO cells when compared to A375 parental cells

2022-01-24 | GSE180568 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data