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The miR-3648/FRAT1-FRAT2/c-Myc feedback loop modulates the metastasis and invasion of gastric cancer cells

ABSTRACT: The miR-3648/FRAT1-FRAT2/c-Myc feedback loop modulates the metastasis and invasion of gastric cancer cells

PROVIDER: PRJNA841874 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19372755_1.fastq.gz	Fastqsanger.gz
	SRR19372755_2.fastq.gz	Fastqsanger.gz
	SRR19372756_1.fastq.gz	Fastqsanger.gz
	SRR19372756_2.fastq.gz	Fastqsanger.gz
	SRR19372757_1.fastq.gz	Fastqsanger.gz

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The miR-3648/FRAT1-FRAT2/c-Myc negative feedback loop modulates the metastasis and invasion of gastric cancer cells.

Project description:Although the abnormal expression of miRNAs in cancer cells is a widely accepted phenomenon, the molecular mechanisms underlying miR-3648 progression and metastasis in gastric cancer (GC) remain unclear. miR-3648 expression is downregulated and its ectopic expression in GC cells significantly suppressed cell proliferation and metastasis. Mechanistic analyses indicated that miR-3648 directly targets FRAT1 or FRAT2 and inhibits FRAT1- or FRAT2-mediated invasion and motility in vitro and in vivo. Moreover, FRAT1 physically interacted with FRAT2. Furthermore, FRAT1 overexpression promoted GC cell invasion, whereas siRNA-mediated repression of FRAT2 in FRAT1-overexpressing GC cells reversed its invasive potential. Besides, miR-3648 inactivated the Wnt/β-catenin signalling pathway by downregulating FRAT1 and FRAT2 in GC. Interestingly, c-Myc, a downstream effector of Wnt/β-catenin signalling, was also downregulated by miR-3648 overexpression. In turn, c-Myc negatively regulated miR-3648 expression by binding to the miR-3648 promoter. In addition, miR-3648 expression levels were negatively correlated with c-Myc, FRAT1, and FRAT2 expression in fresh gastric samples. Our studies suggest that miR-3648 acts as a tumour-suppressive miRNA and that the miR-3648/FRAT1-FRAT2/c-Myc negative feedback loop could be a critical regulator of GC progression.

| S-EPMC9586869 | biostudies-literature

The miR-3648/FRAT1-FRAT2/c-Myc feedback loop modulates the metastasis and invasion of gastric cancer cells

Project description:RNA-seq were used to screen differentially expressed genes in AGS transfected with NC and miR-3648 mimics.

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ZNF252P promotes tumorigenesis by activating c-Myc-mediated positive feedback loop

Project description:Here we screened and identified a novel oncogenic lncRNA, ZNF252P, which is upregulated in a variety of cancer types. ZNF252P promotes cancer cell proliferation and tumorigenicity in vitro and in vivo by activating c-Myc-mediated positive feedback loop. The pivotal regulatory axis of ZNF252P/c-Myc gives it the potential to be the promising biomarker and therapeutic target in cancer development.

2025-01-21 | GSE271524 | GEO

ZNF252P promotes tumorigenesis by activating c-Myc-mediated positive feedback loop

Project description:ZNF252P promotes tumorigenesis by activating c-Myc-mediated positive feedback loop

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A runaway PRH/HHEX-Notch3 feedback loop drives cholangiocarcinoma (ChIP-seq)

Project description:PRH/HHEX-Notch3 feedback loop drives cholangiocarcinoma

2018-12-28 | GSE124430 | GEO

A runaway PRH/HHEX-Notch3 feedback loop drives cholangiocarcinoma (RNA-Seq)

Project description:PRH/HHEX-Notch3 feedback loop drives cholangiocarcinoma

2018-12-28 | GSE124429 | GEO

Invasion control by a positive feedback loop mechanism Smad4-null cells

Project description:New findings demonstrate that transcriptional factors alternative to Smad4 can bind to Smad2/3 and mediate different transcriptional effects. In this study, we detected constitutively phosphorylation of Smad2/3 in Smad4-null pancreatic cancer cell line BxPC-3. Both pan-specific TGF-β-neutralizing antibody and specific TGF-β type I receptor (TβR-I) inhibitor, SB-431542, can decrease steady-state p-Smad2/3 levels. Moreover, exogenous TGF-β strongly stimulated translocation of phosphorylated Smad2/3 (p-Smad2/3) into the nucleus. Therefore, we identified TGF-β-responsive genes using genome-wide oligonucleotide microarrays and confirmed their dependency on Smad2/3 by the combination of RNA interference (RNAi) and microarray assay. The major finding from our microarray analysis was that of the 262 target genes seen to be regulated via TGF-β induction, 87 were differentially transcriptionally controlled by Smad2/3 signaling and 175 were Smad2/3-independent. Our results showed that integrin β6 was transcriptionally up-regulated via TGF-β induction in a Smad3-dependent manner, which was validated by real-time RT-PCR and western blot. We also provide evidence that αVβ6 integrin can activate TGF-β-Smad2/3 signaling. Thus, we for the first time suggest the positive feedback loop compose of TGF-β-Smad3 signaling and integrin β6. Functional analysis revealed that exogenous TGF-β can amplify the invasive property of Smad4-deficient pancreatic cancer cells; however, TGF-β-neutralizing antibody, specific TβR-I inhibitor, and anti-αVβ6 integrin antibody can reduce it. Therefore, integrin β6 mediated the invasion of BxPC-3 cells induced by TGF-β signaling. Keywords: cell type comparison

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A positive feedback loop consisting of C12orf59/NF-κB/CDH11 promotes gastric cancer invasion and metastasis.

Project description:BackgroundMetastasis remains the main cause of cancer-related death for gastric cancer (GC) patients, but the mechanisms are poorly understood. Using The Cancer Genome Atlas (TCGA) data base and bioinformatics analyses, we identified C12orf59 might act as a potential oncogenic protein in GC.MethodsWe investigate the expression pattern and clinical significance of C12orf59 in two independent cohorts of GC samples. In the training cohort, we used the X-tile program software to generate the optimal cutoff value for C12orf59 expression in order to classify patients accurately according to clinical outcome. In the validation cohort, this derived cutoff score was applied to exam the association of C12orf59 expression with survival outcome. A series of in vivo and in vitro assays were then performed to investigate the function of C12orf59 in GC.ResultsC12orf59 was significantly upregulated, and associated with poor survival outcome in two cohorts of GC samples. Gain- and loss of- function studies demonstrated C12orf59 promotes GC cell invasive and metastatic capacity both in vitro and in vivo, and induces epithelial-mesenchymal transition and angiogenesis. Mechanically, C12orf59 exerts oncogenic functions by up-regulating CDH11 expression via NF-κB signaling. Interesting, CDH11 could in turn promote NF-κB bind to C12orf59's promoter and form a positive feedback loop to sustain the metastatic ability of GC cells. Additionally, downregulation of miR-654-5p is another important mechanism for C12orf59 overexpression in GC.ConclusionOur finding suggested the newly identified C12orf59/NF-κB/CDH11 feedback loop may represent a new strategy for GC treatment.

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