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Mus musculus

ABSTRACT: Transcriptome analysis to investigate the oncogenic TGF-β-Smad-Snail signaling pathway

PROVIDER: PRJNA354391 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5034270.fastq.gz	Fastqsanger.gz
	SRR5034271.fastq.gz	Fastqsanger.gz
	SRR5034272.fastq.gz	Fastqsanger.gz
	SRR5034273.fastq.gz	Fastqsanger.gz
	SRR5034274.fastq.gz	Fastqsanger.gz

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Long noncoding RNA ELIT-1 acts as a Smad3 cofactor to facilitate TGF-β/Smad signaling and promote epithelial-mesenchymal transition

Project description:TGF-β is involved in various biological processes, including development, differentiation, growth regulation, and epithelial-mesenchymal transition (EMT). In TGF-β/Smad signaling, receptor-activated Smad complexes activate or repress their target gene promoters. Smad cofactors are a group of Smad-binding proteins that promote recruitment of Smad complexes to these promoters. Long noncoding RNAs (lncRNAs), that behave as Smad cofactors have thus far not been identified. Here, we characterize a novel lncRNA EMT-associated lncRNA induced by TGF-β-1(ELIT-1). ELIT-1 was induced by TGF-β-stimulation via the TGF-β/Smad pathway in TGF-β-responsive cell lines. ELIT-1-depletion abrogated TGF-β-mediated EMT progression and expression of TGF-β target genes including Snail, a transcription factor critical for EMT. A positive correlation between high expression of ELIT-1 and poor prognosis in lung adenocarcinoma and gastric cancer patients suggests that ELIT-1 may be useful as a prognostic and therapeutic target. RIP assays revealed that ELIT-1 bound to Smad3, but not Smad2. In conjunction with Smad3, ELIT-1 enhanced Smad-responsive promoter activities by recruiting Smad3 to the promoters of its target genes including Snail, other TGF-β-target genes, and ELIT-1 itself. Collectively, these data show that ELIT-1 is a novel trans-acting lncRNA that forms a positive feedback loop to enhance TGF-β/Smad3 signaling and promote EMT progression.

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Long noncoding RNA ELIT-1 acts as a Smad3 cofactor to facilitate TGF-β/Smad signaling and promote epithelial-mesenchymal transition

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TGF-β and RREB1 coordinate EMT programs in NMuMG cells

Project description:Epithelial-to-mesenchymal transitions (EMT) play prominent roles during development, regeneration and tumor progression. EMTs are triggered by TGF-β, RAS and other signals that cooperatively induce the expression of master EMT transcription factors such as SNAIL. Here, we elucidate how the TGF-β and RAS pathways jointly trigger EMTs and tie them to broader developmental programs. We identify RAS response element binding protein 1 (RREB1) as a critical partner of TGF-β-activated SMAD transcription factors in driving SNAIL expression and EMT program in mammary gland epithelial cells.

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BAF45D Cooperates with SMAD Signaling and Promotes Early Neural Differentiation in P19 Cells

Project description:We sought to explore whether BAF45D regulates PAX6 expression through cooperating with TGF-beta/SMAD signaling in RA treated P19 cells. Here we identified BAF45D is required for expression of phosphorylated SMAD3 and PAX6 induced by RA. Genome-wide analysis revealed that during RA-induced early neural differentiation, BAF45D knockdown failed to activate TGF-beta/SMAD signaling and induce expression of Stat3 and Smad7, two negative regulators of TGF-beta/SMAD signaling. Moreover, BAF45D was immunoprecipited with BRG1and phosphorylated SMAD3. In addition, Smad3 siRNA abolished RA-indueced expression of phosphorylated SMAD3, PAX6, STAT3 and SMAD7. Finally, overexpression of BAF45D directly induced expression of PAX6 and phosphorylated SMAD3.These results suggest that a novel effect of BAF45D cooperating with TGF-beta/SMAD signaling pathway on PAX6 level control, which may shed new light on neural differentiation of P19 cells.

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Project description:Our study shows that TGF-β signaling promotes tumorigenesis in the liver through upregulation of its target gene, Snail. We explored gene expression changes in tumors following TGF-β inhibition, and tumors ectopically expressing Snail with the TGF-β inhibition. RNA samples were harvested from tumors expressing Smad7 (S7HP tumors), firefly luciferase (LHP tumors), and Smad7 plus Snail (S7HP+Snail), respectively. Differentially expressed genes were investigated in LHP and S7HP+Snail tumors, compared with S7HP tumors.

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SMAD2/3 mediate oncogenic effects of TGF-β in the absence of SMAD4

Project description:The tumor suppressive effects of TGF-β are classically associated with the activation of the “canonical” SMAD-mediated pathway, whereas its oncogenic effects are largely attributed to its “non-canonical signaling”. We herein provide evidence of an oncogenic effect for SMAD2 and 3 in response to TGF-β in SMAD4-null cancer cells. Using the CRISPR/Cas9 technology, we report that simultaneous knockout of Smad2 and 3 in Smad4-negative pancreatic ductal adenocarcinoma (PDAC) cells compromises TGF-β-driven collective migration mediated by FAK and Rho/Rac signaling. Moreover, RNA-sequencing analyses highlight a TGF-β gene signature related to aggressiveness mediated by SMAD2 and 3 in the absence of SMAD4. Using PDAC patients cohorts, we reveal that SMAD4-negative tumors with high levels of (phospho)-SMAD2 are more aggressive and have a poorer prognosis. Thus, loss of SMAD4 tumor suppressive activity in PDAC is associated with oncogenic gain-of-function of SMAD2 and 3 and the onset of associated deleterious effects.

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