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Upregulation of CYR61 by TGF-β and YAP signaling exerts a counter-suppression of hepatocellular carcinoma

ABSTRACT: Upregulation of CYR61 by TGF-β and YAP signaling exerts a counter-suppression of hepatocellular carcinoma

PROVIDER: PRJNA1005202 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25628902_1.fastq.gz	Fastqsanger.gz
	SRR25628902_2.fastq.gz	Fastqsanger.gz
	SRR25628903_1.fastq.gz	Fastqsanger.gz
	SRR25628903_2.fastq.gz	Fastqsanger.gz
	SRR25628904_1.fastq.gz	Fastqsanger.gz

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Upregulation of CYR61 by TGF-β and YAP signaling exerts a counter-suppression of hepatocellular carcinoma

Project description:TGF-β and Hippo signaling are two critical pathways engaged in cancer progression by regulating both oncogenes and tumor suppressors, yet how the two pathways coordinately exert their functions in the development of hepatocellular carcinoma (HCC) remains elusive. In this study, we firstly conducted an integrated analysis of public liver cancer databases and our experimental TGF-β target genes, identifying CYR61 as a pivotal gene relating to HCC development. Evidence revealed that CYR61 is a direct target gene of TGF-β in liver cancer cells. In addition, TGF-β-stimulated Smad2/3 and the Hippo pathway downstream effectors YAP and TEAD4 can form a protein complex on the promoter of CYR61, thereby activating the promoter activity and stimulating CYR61 gene transcription in a collaborative manner. Functionally, depletion of CYR61 enhanced TGF-β- or YAP activation-mediated growth and migration of liver cancer cells. Consistently, ectopic expression of CYR61 was capable of impeding TGF-β- or YAP-induced malignant transformation of HCC cells in vitro, and attenuating HCC xenograft growth in nude mice. Finally, Downregulation of CYR61 expression in HCC tissues than that in normal liver tissues is well associated with a bad clinical outcome in patients. Together, these results add new evidence for the interplay between TGF-β and Hippo signaling and unveil an important tumor suppressor function of CYR61 in liver cancer.

2023-08-19 | GSE240760 | GEO

Downregulation of CYR61 promotes hepatocellular carcinoma progression by ameliorating the protumor functions of TGF-β/YAP and impeding the activation of stromal hepatic stellate cells

Project description:Hepatic stellate cells (HSCs) in the tumor microenvironment play a pivotal role in the development of hepatocellular carcinoma (HCC), which is the major form of primary liver cancers and one of the most lethal cancer types worldwide. TGF-β and Hippo signaling are two critical pathways regulating HSC activation and HCC development through their downstream transcriptional regulators, i.e., Smad proteins and YAP/TEADs, respectively. However, how the two pathways coordinately exert their functions in HCC remains elusive. In this study, we performed integrated analyses of public liver cancer databases and clinical cancer tissues, leading to identification of CYR61 as one of the key candidate genes that may regulate liver cancer progression. TGF-β-activated Smad2/3 and YAP/TEAD4 can form a protein complex to induce CYR61 expression in both cancer cells and stellate cells. As a secreted matricellular protein, CYR61 exerts its tumor suppressor functions via acting on cancer cells directly or regulating the stromal stellate cells. On one hand, CYR61 ameliorates TGF-β- or YAP-mediated liver cancer cell proliferation, colony formation and invasion in vitro, and also tumor growth in nude mice. On the other, CYR61 also impedes cancer cell- or TGF-β-induced stellate cell activation, thereby mitigating the tumor-promoting functions of HSCs as assessed both in vitro and in vivo. In support of its tumor suppressor function, the expression of CYR61 is reduced in HCC tissues and cell lines when compared with their normal counterparts, which is associated with a shorter survival period in cancer patients. Together, these results add new evidence for the interplay between TGF-β and Hippo signaling in regulating gene transcription, and unveil a pivotal role of CYR61 in suppressing liver cancer progression by controlling the activation of hepatic stellate cells in the tumor microenvironment.

2023-01-11 | GSE222402 | GEO

Tetracycline-Inducible Cyr61 effect on LN229 glioma cells

Project description:Glioblastoma multiforme is the most common and aggressive form of brain cancer. The use of oncolytic HSV-1 (oHSV) to selectively target brain cancer cells leading to their lytic destruction has shown to be very promising in a preclinical setting, but is lacking efficacy in clinical trials. Cyr61, a secreted extracellular matrix protein which functions to promote angiogenesis, migration, proliferation and tumorigenesis, was found to be upregulated rapidly following oHSV infection. Here we show, using microarray analysis, that Cyr61 expression leads to the induction of several genes with type 1 interferon function. We show that Cyr61 mediated type 1 IFN induction is through its interaction with integrin alpha6beta1 on the cell surface and results in oHSV inhibition, reducing the efficacy of this therapy. We used microarray to detail the global program of gene expression underlying Cyr61 mediated oncolytic HSV-1 inhibition and identified distinct classes of up-regulated genes during this process. Tetracycline-Inducible glioma cells expressing Cyr61 protein in the presence of doxycycline were treated with or without doxycycline for 24 hours. RNA was extracted and hybridized on Affymetrix microarray. Two groups: Â± dox to induce cyr61, performed in triplicate.

2012-04-03 | E-GEOD-29384 | biostudies-arrayexpress

Tetracycline-Inducible Cyr61 effect on LN229 glioma cells

2012-04-04 | GSE29384 | GEO

RNA-seq of CYR61-treated THP1 human monocytes

Project description:We assess the effects of CYR61 treatment on the transcriptome of human THP1 monocytes.

2023-10-18 | GSE233125 | GEO

CYR61 orchestrates NASH fibrosis through SYK-NFκB-PDGF signaling in monocyte-derived macrophages [bulk RNA-seq]

Project description:Obesity is increasing worldwide and leads to a multitude of metabolic diseases including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatosis (NASH). Here we examine the role of CYR61 in liver fibrosis and inflammation and its potential as a therapeutic target. Loss of CYR61 during NASH injury improves glucose tolerance, decreases liver inflammation and reduces fibrosis. CYR61 activates signaling in monocytes and monocyte-derived macrophages promoting a pro-inflammatory/pro-fibrotic phenotype through a CYR61/SYK/NFKB signaling cascade. In vitro, CYR61 activates Pdgfa and Pdgfb expression in macrophages in a NFκB-dependent manner. Ultimately, we identify a potential therapeutic for NASH: a CYR61-blocking antibody that reduces fibrotic injury and CYR61-driven signaling in macrophages in vitro and in vivo. This study demonstrates that CYR61 is a key driver of liver inflammation and fibrosis and a strong therapeutic target for treatment of NAFLD/NASH.

2023-10-02 | GSE199637 | GEO

CYR61 orchestrates NASH fibrosis through SYK-NFκB-PDGF signaling in monocyte-derived macrophages [HIVE single-cell RNA-seq]

2023-10-02 | GSE199639 | GEO

CYR61 orchestrates NASH fibrosis through SYK-NFκB-PDGF signaling in monocyte-derived macrophages [10X single-cell RNA-seq]

2023-10-02 | GSE199638 | GEO

Bulk RNA-seq of: HUVECs co-incubated with CYR61-treated mouse bone marrow-derived macrophages CYR61-treated murine bone marrow-derived macrophages CYR61-treated HUVECs and CYR61-treated human THP1 monocytes

Project description:Bulk RNA-seq of: HUVECs co-incubated with CYR61-treated mouse bone marrow-derived macrophages CYR61-treated murine bone marrow-derived macrophages CYR61-treated HUVECs and CYR61-treated human THP1 monocytes

| PRJNA917714 | ENA

RNA-seq of CYR61-treated human umbilical vein endothelial cells

Project description:We assess the effect of CYR61 treatment on the transcriptome of human umbilical vein endothelial cells.

2023-10-18 | GSE222101 | GEO