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Gene expression profiles after knockdown of Nardilysin in TMK-1 gastric cancer cells

ABSTRACT: Nardilysin (NRDc), a metalloendopeptidase of the M16 family, has been reported to promote the ectodomain shedding and resulting activation of various growth factors and cytokines, but its role in cancer biology have not been elucidated. Microarray experiments were performed to analyze the chnages of gene expression profiles after knockdown of NRDc by microRNA (miR)-based RNA interference (RNAi).

ORGANISM(S): Homo sapiens

PROVIDER: GSE29144 | GEO | 2011/05/16

SECONDARY ACCESSION(S): PRJNA140349

REPOSITORIES: GEO

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Gene expression profiles after knockdown of Nardilysin in TMK-1 gastric cancer cells

Project description:Nardilysin (NRDc), a metalloendopeptidase of the M16 family, has been reported to promote the ectodomain shedding and resulting activation of various growth factors and cytokines, but its role in cancer biology have not been elucidated. Microarray experiments were performed to analyze the chnages of gene expression profiles after knockdown of NRDc by microRNA (miR)-based RNA interference (RNAi). RNAi experiments were perfomed using BLOCK-iT Pol II miR RNAi Expression Vector Kit with EmGFP (Invitrogen). TMK-1 cells stably expressing conrol or NRDc-targeting miR vector were established.

2011-05-16 | E-GEOD-29144 | biostudies-arrayexpress

Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction

Project description:Myocardial infarction (MI) contributes to cardiac mortality and morbidity. After myocardial infarction the innate immune response is pivotal in clearing of tissue debris as well as scar formation, but exaggerated cytokine and chemokine secretion with subsequent leukocyte infiltration also leads to further tissue damage. Post-translational regulation of cytokine / chemokine signaling occurs via ectodomain shedding through a disintegrin and metalloproteases (ADAMs). Here, we address the value of targeting a previously unknown ADAM10 / CX3CL1 axis in the regulation of neutrophil recruitment early after MI. We show that myocardial ADAM10 is distinctly upregulated in biopsies from patients with ischemia-driven cardiomyopathy and correlates with heart failure progression. Intriguingly, upon MI in mice, pharmacological treatment with the ADAM10 inhibitionor GI254023X as well as genetic cardiomycyte-specific ADAM10 deletion improves survival with markedly enhanced heart function and reduced scar size. Mechanistically, this is driven by abolished ADAM10-mediated CX3CL1 ectodomain shedding followed by diminished IL-1β-dependent inflammation, reduced neutrophil bone marrow egress as well as myocardial tissue infiltration. Genetic cardiomycyte-specific ADAM10 deletion confirmes the small-molecule data and leads to improved cardiac function and reduction in inflammatory markers after ischemic myocardial injury. Thus, our data shows a conceptual insight into how acute MI induces chemotactic signaling via ectodomain shedding in cardiomyocytes.

2022-11-10 | GSE217268 | GEO

Microarray analysis of primary human basal cell carcinoma, squamous cell carcinoma, and normal skin

Project description:We used RNA microarray to investigate the expression of full-time and part-time sheddases and their substrates in basal cell carcinoma when compared to squamous cell carcinoma and normal skin. We aimed to identify the involvement of these sheddases in CD200 ectodomain shedding. RNA was extracted from whole primary tissues and sent for sequencing. raw sequencing data was then processed in R using 'lumi' and 'limma' packages.

2022-08-25 | E-MTAB-12034 | biostudies-arrayexpress

Gene expression profiling for: activin-2 is required for regeneration of polarity on the planarian anterior-posterior axis

Project description:The goal of this data set is to identify transcriptional changes in activin-2 RNAi animals vs control animals. We did bulk RNA sequencing of a wound induced time course to try to identify changes in the context of activin-2 RNAi, and targets of activin-2. These changes may help explain some of the phenotypic chnages seen in activin-2 RNAi animals.

2020-05-15 | GSE148376 | GEO

Degradome of soluble ADAM10 and ADAM17 metalloproteases

Project description:Disintegrin and metalloproteinases ADAM10 and ADAM17 can release the extracellular region of a variety of membrane-bound proteins including cytokines, adhesion molecules, growth factors and receptors, important for many biological functions (ectodomain shedding).. So far, substrate identification for ADAM10 and ADAM17 focused exclusively on their membrane-anchored forms and their function as sheddases. With ADAM8 we now describe the first protease capable of releasing the ADAM17 ectodomain. Based on these findings, we investigated whether the soluble ectodomains of ADAM10 and ADAM17 still exhibit shedding activity and to determine their soluble protein substrate pool . To address this, a mass spectrometry-based N-terminomics approach (TAILS) was used to identify potential targets of soluble ADAM10 and ADAM17 (sADAM10/17) within the secretome of the murine cardiomyocyte cell line HL-1. We identified almost 140 protein cleavage events in total and 45 common substrates for both sADAM10 and sADAM17. Further in-vitro studies confirmed fibronectin, cystatin C, sN-cadherin, PCPE-1 as well as sAPP as direct substrates of soluble ADAM10 and/or ADAM17. Overall, we present the first degradome study for sADAM10 and sADAM17, thereby introducing a new regulation mode of the proteolytic activity of these essential proteases within the protease web.

2019-06-24 | PXD013718 | Pride

Heparan sulfate modifications of betaglycan promote TIMP3-dependent ectodomain shedding to fine-tune TGF-β signaling.

Project description:Betaglycan/type III TGF-β receptor (TGFBR3) is an established co-receptor for the TGF-β superfamily with direct binding demonstrated for TGF-β 1-3 and inhibin A. Betaglycan can be membrane-bound or have its ectodomain cleaved/ shed to produce soluble-betaglycan that has been demonstrated to sequester ligands. Extracellular domain of betaglycan is modified with glycosaminoglycan chains at Ser residues S534 and S545, to which heparan sulfate and chondroitin sulfate chains are covalently attached. To delineate the contribution of the heparan and chondroitin sulfate modifications on betaglycan on its shedding and thereby on TGF-β signaling in ovarian cancer biology, we used mutants of betaglycan with alterations to the different glycosaminoglycan modifications. We made the unexpected discovery that the heparan sulfate modifications are essential for maximum ectodomain shedding of betaglycan, which is further essential for the ability of betaglycan to suppress TGF-β signaling and the tumor cells responses to exogenous TGF-β ligand. Using unbiased transcriptomics, we identified TIMP3 as a key regulator of betaglycan shedding and thereby TGF-β signaling. Taken together, these studies are the first to demonstrate a critical link between the well-known modifications on betaglycan and TGF-β signaling responses.

2024-02-21 | GSE237403 | GEO

System-wide vitreous proteome dissection reveals impaired sheddase activity in diabetic retinopathy

Project description:Diabetic retinopathy (DR) is a major complication of diabetes mellitus causing significant vision loss. Despite the success of anti-VEGF therapy as an effective therapy, many DR patients do not respond well to the treatment, emphasizing the involvement of other molecular players. To unveil these, we performed deep vitreous proteome profiling of patients with proliferative DR and extracted aberrated protein networks. This revealed impairment in ectodomain shedding of several transmembrane proteins playing critical roles in neurodegeneration and angiogenesis, that pointed to defects in their regulating sheddases, particularly ADAM10, which emerged as the predominant sheddase. We confirmed that ADAM10 protease activity was reduced in ocular disease models and established that activation of ADAM10 can suppress endothelial cell activation and angiogenesis. Furthermore, we identified impaired ADAM10-AXL axis as a retinal angiogenic driver. Taken together, we demonstrate restoration of aberrant ectodomain shedding as an effective strategy for treating DR and propose ADAM10 as an attractive novel target.

2022-10-14 | PXD036033 | Pride

Proteolytic processing of CD99

Project description:The adhesion molecule CD99 is essential for transendothelial migration (TEM) of leukocytes. Here we demonstrate by biochemical and cellular assays that CD99 undergoes ectodomain shedding by the metalloprotease meprin β and subsequent intramembrane proteolysis by γ-secretase. The cleavage site in CD99 was identified by mass spectrometry within an acidic region highly conserved through different vertebrate species.

2017-01-02 | PXD005428 | Pride

HAVCR/KIM-1 activates the IL-6/STAT-3 Pathway in ccRCC and Determines Tumor Progression and Patient Outcome

Project description:Renal cell carcinoma (RCC), the third most prevalent urological cancer, claims more than 100,000 lives/year worldwide. The clear cell (ccRCC) is the most common and aggressive subtype of renal cancer. Commonly asymptomatic, more than 30% of ccRCCs are diagnosed when they are already metastatic resulting in a 95% mortality rate and one-third of organ-confined cancers treated by nephrectomy develop metastasis during the follow-up. Diagnosis and monitoring requires expensive and frequent imaging examinations; thereby, finding of diagnostic and prognostic biomarkers to screen, diagnose and monitor renal cancers are clearly needed. Hepatitis A virus receptor/kidney injury molecule 1 (HAVCR1/KIM-1) gene has been claimed to be a susceptibility gene for ccRCC and HAVCR1/KIM-1 ectodomain shedding a predictive biomarker of tumor progression.

2020-09-27 | E-MTAB-2071 | biostudies-arrayexpress

SLC25A25-AS1 knockdown data of two colorectal carcinoma cell lines (HT29 and SW480)

Project description:We identified that SLC25A25-AS1 was a lncRNA influencing radiation response. Therefore, we aimed to explore more biological roles of SLC25A25-AS1 in this process. Towards this end, we used RNA interference (RNAi)-mediated knockdown of SLC25A25-AS1 in HT29 and SW480 to explore the changes of mRNA expression profiles and explore the phenotype outcomes.

2017-03-03 | GSE95605 | GEO

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