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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Girish Patel

PROVIDER: E-MTAB-12034 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Microarray analysis of the NK92MI cell line treated with CD200 peptide at 2hr and 4hr timepoints compared to untreated

Project description:We used RNA microarray to investigate CD200-mediated apoptosis on the NK92MI celll line. We aimed to identify apoptotic gene signatures. RNA was extracted from NK92MI cells and sent for sequencing. raw sequencing data was then processed in R using 'lumi' and 'limma' packages.

2022-08-25 | E-MTAB-12035 | biostudies-arrayexpress

Quantitative secretome analysis using improved secretome-protein-enrichment-with-click-sugars method (iSPECS) establishes the cell type-resolved mouse brain glyco-secretome

Project description:To understand how cells communicate with each other, it is essential to define the cellular secretome, a collection of proteins including soluble secreted, unconventionally secreted and proteolytically-shed proteins. Quantitative methodologies to decipher the secretome are challenging, due to the requirement of large cell numbers and abundant serum proteins that interfere with the detection of low-abundant cellular secretome proteins. Here, we miniaturized secretome analysis by developing the improved secretome-protein-enrichment-with-click-sugars method (iSPECS), which identifies the glyco-secretome. We applied this method to provide a cell type-resolved mouse brain glyco-secretome resource. Our data show that a surprisingly high number of secreted proteins are generated by ectodomain shedding in a cell type-specific manner. Two examples are neuronally secreted ADAM22 and CD200, which we identified as new substrates of the Alzheimer-linked protease BACE1. Taken together, iSPECS and the brain glyco-secretome resource can be exploited for a wide range of applications to study protein secretion and shedding.

2020-09-25 | PXD018171 | 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

The CD200-CD200R axis promotes squamous cell carcinoma metastasis via regulation of Cathepsin K

Project description:The CD200-CD200R immunoregulatory signaling axis plays an etiological role in the survival and spread of numerous cancers primarily through suppression of anti-tumor immune surveillance. Our previous work outlined a pro-metastatic role for the CD200-CD200R axis in cutaneous squamous cell carcinoma (cSCC) that is independent of direct T cell suppression but modulates the function of infiltrating myeloid cells. To identify effectors of the CD200-CD200R axis important for cSCC metastasis, we conducted RNA-Seq profiling of infiltrating CD11b+Cd200r+ cells isolated from Cd200+ versus Cd200 null cSCCs and identified the cysteine protease Cathepsin K (Ctsk) to be highly upregulated in Cd200+ cSCCs. CD11b+Cd200r+ cells, which expressed phenotypic markers associated with myeloid-derived suppressor cell-like cells and tumor-associated macrophages, were the primary source of Ctsk expression in cSCC. Using a Cd200r+ myeloid cell-cSCC co-culture system, we observed that induction of Ctsk in Cd200r+ tumor-infiltrating cells was dependent on engagement of the CD200-CD200R axis, indicating that Ctsk is a target gene of this pathway in the cSCC tumor microenvironment. Inhibition of Ctsk, but not matrix metalloproteinases (MMPs), significantly blocked cSCC cell migration through collagen gels in vitro. Finally, both targeted Cd200 disruption in tumor cells and Ctsk pharmacological inhibition dramatically reduced cSCC metastasis in vivo. Collectively, our findings identify a novel direct role for Cd200r+ infiltrating myeloid lineages in tumor metastasis and support the conclusion that CD200 stimulates cSCC invasion and metastasis via induction of Ctsk in CD200r+ infiltrating cells.

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Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction

Project description:Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction

| PRJNA898315 | ENA

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

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

2011-05-16 | GSE29144 | GEO

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

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