Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RAVER1 interconnects TGFB signaling, EMT and miR/RISC activity by modulating alternative splicing [A549_RAVER1_KD]

ABSTRACT: RAVER1 interconnects TGFB signaling, EMT and miR/RISC activity by modulating alternative splicing [A549_RAVER1_KD]

PROVIDER: PRJNA973631 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

RAVER1 interconnects lethal EMT and miR/RISC activity by the control of alternative splicing

Project description:The RAVER1 protein was proposed to serve as a co-factor in guiding the PTBP-dependent control of alternative splicing (AS). Whether RAVER1 solely acts in concert with PTBPs and how it affects cancer cell fate remained elusive. Here we provide the first comprehensive investigation of RAVER1-controlled AS in cancer cell models and reveal a pro-oncogenic role of RAVER1 in tumor growth. This unravels that RAVER1 guides AS in synergy with PTBPs but more prominently serves PTBP1-independent roles in splicing. In cancer cells, one major function of RAVER1 is the control of proliferation and apoptosis, which involves the modulation of AS events within the miR/RISC pathway. Associated with this regulatory role, RAVER1 antagonizes lethal, TGFB-driven epithelial-mesenchymal-transition (EMT) by limiting TGFB signaling. RAVER1-modulated splicing events affect the insertion of protein interaction modules in factors guiding miR/RISC-dependent gene silencing. Most prominently, in all three human TNRC6 proteins, RAVER1 controls AS of GW-enriched motifs, which are essential for AGO2-binding. Disturbance of RAVER1-guided AS events in TNRC6 proteins and other facilitators of miR/RISC activity compromise miR/RISC activity which is essential to restrict TGFB signaling and lethal EMT.

2024-01-11 | PXD043342 | Pride

RAVER1 interconnects TGFB signaling, EMT and miR/RISC activity by modulating alternative splicing [A549_RAVER1_KD]

Project description:The depletion and deletion of RAVER1 substantially impairs the 2D-proliferation of tumor cells, vitality in 3D cell models and the growth of subcutaneous xenografts in nude mice. Disturbance of RAVER1 affects various cancer hallmark pathways manifesting in deregulated E2F/DREAM-controlled transcription and broadly hampered microRNA-dependent gene silencing. In carcinoma-derived cell models, impaired control by microRNAs (miR) leads to the upregulation of various tumor suppressors like BTG2, which is suppressed by the most abundant oncomiR 21-5p.

2023-06-14 | GSE232714 | GEO

Transcriptome of EMT induced MCF10A cells by TGFb treatment or SNAIL S6A expression.

Project description:EMT, Epithelial to mesenchymal transition is a developmental biology process associated with migration, known to be involved in cancer metastasis. To study this process, we used the breast epithelial cell line MCF10A that enter in EMT after treatment with the cytokine TGFB or by expression of EMT transcriptor factor SNAIL.

2017-01-30 | GSE89152 | GEO

Gene expression profiling of NSCLC cell lines upon TGFb-induced epithelial-mesenchymal transition (EMT)

Project description:Epithelial-mesenchymal transition has been implicated in tumor metastasis, cancer drug resistance and cancer stem cell features. In this study, we examined gene expression profiles of three non-small cell lung cancer cell lines, before and after experimentally induced EMT. We modeled epitheial-mesenchyml transition by culturing A549, HCC827 and NCI-H358 cells in the presence of TGFb for three weeks, and compared gene expression profiles of the paretnal cells and cells after EMT.

2014-11-19 | E-GEOD-49644 | biostudies-arrayexpress

WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [ChIP-seq]

Project description:The core subunit of the COMPASS-like complex, WD Repeat Domain 5 (WDR5) has a prominent role in reprogramming and Epithelial-to-Mesenchymal transition (EMT) in different tumor types. Our evidences support a model in which WDR5 is prominent for EMT and metastasis dissemination in breast cancer patient-derived xenografts and cell lines. Moreover, WDR5 silencing abrogates TGFB pathway activation and reverts mesenchymal into epithelial phenotype, by inhibiting transcription of main master regulators of EMT (CDH2, TWIST1, SNAI1, SNAI2 and ZEB1). Our data suggest that WDR5 inhibition may be a successful approach to prevent progression of metastatic BC.

2019-12-17 | GSE113279 | GEO

WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq CCL]

2019-12-17 | GSE113283 | GEO

WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway [RNA-seq PDX]

2019-12-17 | GSE113288 | GEO

WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway

Project description:WDR5 regulates EMT and metastasis in breast cancer by activating TGFB pathway

| PRJNA450652 | ENA

TGFb-induced transcriptome profile in cancer cell lines

Project description:TGFb plays many roles during tumor progression. It inhibits epithelial cell proliferation in the early stage but promotes tumor invasion by inducing epithelial-to-mesenchymal transition (EMT) in the late stage. Coupled with the strong EMT effect, TGFb exerts an overwhelming influence on modifying the extracellular matrix (ECM), which is generally thought to favor the adhesion and migration of tumor cells [4]. However, the regulation and function of ECM deposited in the tumor microenvironment by TGFb signaling have not been elucidated. Here, we performed a transcriptomic analysis using the human prostate cancer PC3U cell line and the human A549 lung carcinoma cell line. The top-upregulated genes in PC3U cells and A549 cells upon TGFb stimulation were identified to analyze the main regulatory function elicited by TGFb signaling. The GO enrichment analysis showed that extracellular matrix organization and the positive regulation of cell migration were the top regulatory functions.

2024-09-12 | GSE274287 | GEO

TGFb treated EpRAS cells undergoing hysteretic vs non-hysteretic EMT gene expression analysis.

Project description:TGFb treated EpRAS cells undergoing hysteretic vs non-hysteretic EMT gene expression analysis.

| PRJNA417150 | ENA