Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene profiling in carcinoma cell during EMT

ABSTRACT: Modulation of several waves of gene expression during FGF-1 induced Epithelial-mesenchymal transition of carcinoma cells . In vitro FGF-1 induced EMT study using NBTII rat bladder carcinoma cells Keywords: time course ; EMT ; cancer cell line ; FGF-1

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE5664 | GEO | 2008/02/20

SECONDARY ACCESSION(S): PRJNA96939

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of rat Fcarcinoma cells during FGF-1 induced Epithelial-mesenchymal transition

Project description:Modulation of several waves of gene expression during FGF-1 induced Epithelial-mesenchymal transition of carcinoma cells . In vitro FGF-1 induced EMT study using NBTII rat bladder carcinoma cells Experiment Overall Design: NBTII and NBTII-FGFR1 cells were induced by FGF-1. Total RNA were prepared from stimulated and control cells at time 0.5, 2, 6, 24 and 48 hours. Except for control and 0.5 hour stimulated cells, the experiment was done in duplicate for each cell line type

2008-04-07 | E-GEOD-5664 | biostudies-arrayexpress

PRMT5 circular RNA promotes the metastasis of urothelial carcinoma of the bladder cells through sponging miR-30c to induce epithelial-mesenchymal transition

Project description:We are using circRNA expression profiling to identify novel circular RNA regulating EMT progression in urothelial carcinoma of the bladder.

2021-04-04 | GSE112719 | GEO

RhoJ controls EMT associated resistance to chemotherapy

Project description:The resistance of cancer cells to therapy is responsible for the death of most cancer patients. Epithelial-to-mesenchymal transition (EMT) has been associated with resistance to therapy in different cancer cells. However, the mechanisms by which EMT mediates resistance to therapy remain poorly understood. Here, using a mouse model of skin squamous cell carcinoma (SCC) undergoing spontaneous EMT during tumorigenesis, we found that EMT tumor cells were highly resistant to a wide range of anti-cancer therapy both in-vivo and in-vitro. Using gain and loss of function in vitro and in vivo, we uncovered that RhoJ, a small GTPase preferentially expressed in EMT cancer cells, controls resistance to therapy. Using genome-wide transcriptomic and proteomic profiling, we found that RhoJ regulates EMT associated resistance to chemotherapy by promoting DNA damage response and the formation of new replication forks allowing tumor cells to repair DNA lesions more rapidly and survive under the replicative stress induced by chemotherapy. Using affinity-purification followed by mass spectrometry, we found that RhoJ interacts with proteins regulating nuclear actin and the inhibition of actin polymerization sensitizes EMT tumor cells to chemotherapy induced cell death in a Rhoj dependent manner. Altogether, our study uncovers the role and the mechanisms by which RhoJ acts as a key regulator of EMT associated resistance to chemotherapy.

2023-01-13 | PXD038278 | Pride

RhoJ controls EMT associated resistance to chemotherapy

Project description:The resistance of cancer cell to therapy is responsible of the death of most cancer patients. Epithelial to mesenchymal transitions (EMT) has been associated with resistance to therapy in different cancer cells. However, the mechanisms by which EMT mediates resistance to therapy remain poorly understood. Here, using a mouse model of skin squamous cell carcinoma (SCC) undergoing spontaneous EMT during tumorigenesis, we identified EMT tumor subpopulations displaying different intrinsic resistance mechanisms to a wide range of anti-cancer therapy both in-vivo and in-vitro. We found that RhoJ, a small GTPase, preferentially expressed in EMT cancer cells controls resistance to therapy. Using genome-wide transcriptomic and proteomic profiling combined with functional assays following loss of RhoJ functions, we found that RhoJ regulated EMT associated resistance to chemotherapy by promoting DNA damage response and the formation of new replication forks allowing EMT tumor cells to repair DNA lesions more rapidly and survive under the replicative stress induced by chemotherapy. Altogether, our study uncovers RhoJ as a key regulator of EMT associated resistance to chemotherapy with important implications for the development of new strategies to overcome resistance to therapy in cancer.

2023-01-13 | PXD025737 | Pride

Dysregulation of EMT Drives the Progression to Clinically Aggressive Sarcomatoid Bladder Cancer

Project description:The progression of conventional urothelial carcinoma (UC) of the bladder to a tumor with a mesenchymal phenotype, referred to as sarcomatoid carcinoma (SARC), is signified by a high propensity for regional and distant metastasis resulting in shorter survival. We report a comprehensive retrospective analysis of 28 cases of SARCs and 84 cases of conventional UCs. A TCGA cohort of 408 muscle-invasive bladder cancers was used as a reference cohort. SARCs showed a distinct mutational landscape with enrichment of p53, PIK3CA, and RB1 mutations. They developed from basal precursor conventional UCs and could be divided into a basal subtype and the most aggressive mesenchymal subtype. Expression analysis showed that SARCs are driven by dysregulation of cell cycle and EMT regulatory networks and nearly half exhibited an immune infiltration phenotype with PDL1 upregulation. Our observations have important implications for prognostication and the development of more effective therapies for this highly lethal variant of bladder cancer.

2019-05-07 | GSE128192 | GEO

Calcium signaling induces a partial EMT in carcinoma cells

Project description:Calcium signaling induces a partial EMT in carcinoma cells

| PRJNA663298 | ENA

Dysregulation of EMT Drives the Progression to Clinically Aggressive Sarcomatoid Bladder Cancer [RT-PCR]

2019-03-14 | GSE128277 | GEO

Tumor Stemness Score to Estimate Epithelial-to-Mesenchymal Transition (EMT) and Cancer Stem Cells (CSCs) Characterization and to Predict the Prognosis and Immunotherapy Response in Bladder Urothelial Carcinoma

Project description:Background: The relationships between cancer stem cells (CSCs), epithelial-to-mesenchymal transition (EMT), and the tumor microenvironment (TME) in bladder urothelial carcinoma (BLCA) remain unclear. Methods: We first constructed tumor stemness (TS) score using principal component analysis to quantify tumor stemness in BLCA. Then, we evaluated the clinical value of the TS score for predicting the response to tumor immunotherapy using immunotherapy cohorts. Finally, we built an EMT cell model by treating T24 cells with TGF-β and validated the relationship between the TS score and the EMT process in tumors by real-time quantitative PCR, cell invasion assays, and RNA-seq. Results: A TS scoring system was established with 61 TS-related genes to quantify the TS. The prognostic value of the TS score was then confirmed in multiple independent cohorts. A high TS score was associated with high EMT activity, CSC characteristics, high stromal cell content, high TP53 mutation rate, poor prognosis, and high tumor immunotherapy tolerance. Conclusion: The TS score provides an index for EMT and CSC research and helps clinicians develop treatment plans and predict outcomes for patients.

2022-10-21 | GSE215947 | GEO

Profiling of EMT-associated mitochondrial RNAs in hepatocellular carcinoma cells

Project description:Mitochondria, the powerhouse of the cell, has been recognized as the key players in cancer cell biology, including cancer metabolism, metastasis, and drug resistance. Recent studies have demonstrated a functional interplay between mitochondria and epithelial-mesenchymal transition (EMT) in cancer. To delineate the role of mitochondrial components in this interplay, we induced the EMT in hepatoma HepG2 cells. Mitochondria was isolated from EMT-HepG2 cells, untreated HepG2 cells, and normal hepatic HL7702 cells. Mitochondrial RNAs were isolated for Illumina sequencing. Identification of mitochondrial RNAs that regulate EMT or mitochondria function may serve as potential therapeutic targets for developing new strategies to treat cancers.

2019-08-27 | GSE119946 | GEO

Profiling of EMT-associated mitochondrial RNAs in hepatocellular carcinoma cells

Project description:Profiling of EMT-associated mitochondrial RNAs in hepatocellular carcinoma cells

| PRJNA490756 | ENA