Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profile in SK-LM_S1 cells mediated by abrogation of MAPK7 and VCAN gene expression [Part 1]

ABSTRACT: The ERK5 signaling pathway has emerged as a novel key player in soft tissue sarcoma biology, mediating tumour growth and progression. Here we show how the expression of VCAN, a member of the chondroitin sulphate proteoglycan family, is modulated by the ERK5 pathway at the transcriptional level and mediates biological processes such as migration, adhesion, proliferation and tumourigenesis in vivo. This conclusion is based on genetic (shRNA, overexpression) and pharmacological approaches using the human soft tissue sarcoma cell lline Sk-LM-S1 a. In particular, VCAN knockdown mimics ERK5 knockdown in vitro and in vivo, whereas VCAN overexpression restores the phenotypes observed after ERK5 knockdown. In addition, transcriptomic studies show that VCAN is a central mediator in the ERK5-associated transcriptional landscape, supporting its role in diverse biological processes. Taken together, these data support VCAN as a new key target in the ERK5 pathway.

ORGANISM(S): Homo sapiens

PROVIDER: GSE289613 | GEO | 2026/02/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-Seq study of cartilage tissue regeneration in vivo using a biomimetic 3D scaffold

Project description:Analysis of transcriptome changes in rabbit cartilage tissue following surgical induction of critical size defects on knee joints with or without collagen-chondroitin sulphate (CLCS) 3D scaffolds.

2021-12-07 | GSE149098 | GEO

Deep transcriptome analysis of mouse embryonic fibroblast following simultaneous overexpression of Stella, Oct4 and Nanos2 (SON)

Project description:We constructed a polycistronic lentiviral vector to overexpress 3 germ cell specific genes (Stella, Oct4 and Nanos2) in mouse embryonic fibroblast (MEFs) and evaluated the transcriptome portrait in partially reprogrammed cells.We sequenced RNA samples from bulk cell population of two biological duplicates of MEF-GFP (control) and MEF-SON (overexpressed) 21 days post infection. Differential expression analysis of 50 M pair-end read per samples showed overexpression of neurogenesis, blood vessel and proliferation related genes and downregulation of chondroitin sulphate metabolic process, nitric oxide production and innate immune response genes. Examination of whole transcriptome following concurrent overexpression of Stella, Oct4 and Nanos2 in MEFs.

2016-07-30 | E-GEOD-77351 | biostudies-arrayexpress

Deep transcriptome analysis of mouse embryonic fibroblast following simultaneous overexpression of Stella, Oct4 and Nanos2 (SON)

2016-07-30 | GSE77351 | GEO

MicroRNA-590-3p promotes ovarian cancer growth and metastasis via a novel FOXA2-Versican pathway

Project description:Epithelial ovarian cancer (EOC) is the deadliest gynecological cancer. MicroRNAs (miRNAs) are small non-coding RNAs that play important roles in gene regulation and their dysregulation is associated with many diseases. In this study, we determined the expression and function of miR-590-3p in EOC. We found that miR-590-3p levels were higher in high-grade carcinoma when compared to low-grade or tumours with low malignant potential. Interestingly, plasma levels of miR-590-3p were significantly higher in EOC patients than in subjects with benign gynaecological disorders. Transient transfection of miR-590-3p mimics, or stable transfection of mir-590, increased cell growth, migration, and invasion. In vivo studies revealed that mir-590 accelerated tumour growth and metastasis. Using a cDNA microarray, we identified Forkhead box A2 (FOXA2) and Versican (VCAN) as a top downregulated and a top upregulated gene, respectively, by mir-590. We showed that miR-590-3p targeted FOXA2 3’ UTR to suppress its expression. In addition, knockdown of FOXA2 by siRNAs or knockout of FOXA2 by CRISPR/Cas9 enhanced cell proliferation, migration, and invasion. Overexpression of FOXA2 decreased, while knockout of FOXA2 increased, VCAN mRNA and protein levels and ChIP-qPCR revealed that FOXA2 binds to VCAN promoter. Interrogation of the TCGA ovarian cancer database revealed a negative relationship between FOXA2 and VCAN mRNA levels in EOC tumours and that high FOXA2/low VCAN mRNA levels in tumours were positively correlated with patient survival. Finally, overexpression of FOXA2 or silencing of VCAN reversed the effects of mir-590. These findings demonstrate that miR-590-3p promotes EOC development via a novel FOXA2-VCAN pathway.

2018-04-21 | GSE113440 | GEO

Acute pharmacological degradation of ERK5 does not inhibit cellular immune response or proliferation

Project description:Over the past few decades, interest in the role that extracellular signal-regulated kinase 5 (ERK5) plays in various diseases, particularly cancer and inflammation, has grown. Phenotypes observed from genetic knockdown or deletion of ERK5 suggested that targeting ERK5 could have therapeutic potential in various disease settings, motivating the development of potent and selective ATP-competitive ERK5 inhibitors. However, these inhibitors were unable to recapitulate the effects of genetic loss of ERK5, suggesting that ERK5 may have key kinase-independent roles. To investigate potential non-catalytic functions associated with ERK5, we report here the development of INY-06-061, a potent and selective heterobifunctional degrader of ERK5. In contrast to results reported through genetic knockdown of ERK5, INY-06-061-induced ERK5 degradation did not induce anti-proliferative effects in multiple cancer cell lines or suppress inflammatory responses in primary endothelial cells. Thus, we have developed and characterized a chemical tool useful for validating phenotypes reported to be associated with genetic ERK5 ablation and for guiding future ERK5-directed drug discovery efforts.

2022-10-13 | PXD036104 | Pride

Acute pharmacological degradation of ERK5 does not inhibit cellular immune response or proliferation

2022-10-13 | PXD036105 | Pride

The Landscape of N6-Methyladenosine in Localized Primary Prostate Cancer

Project description:To investigate the molecular role of VCAN in prostate cancer, we knockdown the VCAN gene by two different shRNAs in PC-3 xenografts.

2024-11-30 | GSE220432 | GEO

The signalling axis ERK5/KLF2 is a major determinant of chemical sarcomagenesis

Project description:Sarcomas are a heterogeneous group of tumors in which the role of ERK5 is poorly studied. To clarify the role of this particular MAPK in sarcomatous pathology, we used a murine 3-methyl-cholanthrene (3MC)-induced sarcoma model. Our data show that 3MC induces pleomorphic sarcomas with muscle differentiation, showing an increased expression of ERK5. Indeed, this upregulation was also observed in human sarcomas of muscular origin such as leiomyosarcoma or rhabdomyosarcoma. Moreover, in cell lines derived from these 3MC-induced tumors, abrogation of Mapk7 expression by using specific shRNAs decreased in vitro growth, colony-forming capacity, and caused a marked loss of tumor growth in vivo. Indeed, the transcriptomic profile in ERK5 abrogated cell lines by RNAseq showed a deregulated gene expression pattern for key biological processes such as angiogenesis, migration or motility, among others. Finally, among the various differentially expressed genes, Klf2, a direct target of the ERK5 pathway, is a key mediator of the biological effects of ERK5 in vitro and in vivo, as indicated by its specific interference. Therefore, our data suggest that the ERK5KLF2 signaling axis is an important determinant of 3MC-induced sarcomas and should be further studied in human sarcomas, especially those of muscular origin.

2022-08-03 | GSE199395 | GEO

Circular RNAs impinge on non-cell-autonomous mechanisms to regulate tumorigenesis. [RNA-seq]

Project description:We report transcriptomic changes in mouse soft-tissue sarcoma cells upon knock-down of the endogenous circRNA, circCsnk1g3. We find that circCsnk1g3 knockdown results in upregulation of signaling pathways related to both production of and response to type-I and type-II interferons

2022-10-20 | GSE163033 | GEO

Subtype-specific genomic alterations define new targets for soft tissue sarcoma therapy

Project description:This SuperSeries is composed of the following subset Series: GSE21122: Whole-transcript expression data for soft-tissue sarcoma tumors and control normal fat specimens GSE21123: Affymetrix SNP array data for soft tissue sarcoma samples Refer to individual Series

2010-07-05 | E-GEOD-21124 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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