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Dynamic interaction- and phosphoproteomics of CD147

ABSTRACT: Using affinity purification, mass spectrometry, and phospho-enrichment of isotope-labeled peptides, we examined the CD147 microenvironment and CD147-dependent signaling cascades in the Jurkat acute T cell leukemic cell line and its dynamics upon treatment with T cell stimulating agents.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Nagarjuna Nagaraj

LAB HEAD: Hannes Stockinger

PROVIDER: PXD002055 | Pride | 2017-02-06

REPOSITORIES: pride

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			Action	DRS
	Orbi1_0908_01.RAW	Raw
	Orbi1_0908_02.RAW	Raw
	Orbi1_0908_03.RAW	Raw
	Orbi1_0908_04.RAW	Raw
	Orbi1_0908_05.RAW	Raw

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Publications

Dynamic Interaction- and Phospho-Proteomics Reveal Lck as a Major Signaling Hub of CD147 in T Cells.

Supper Verena V Hartl Ingrid I Boulègue Cyril C Ohradanova-Repic Anna A Stockinger Hannes H

Journal of immunology (Baltimore, Md. : 1950) 20170201 6

Numerous publications have addressed CD147 as a tumor marker and regulator of cytoskeleton, cell growth, stress response, or immune cell function; however, the molecular functionality of CD147 remains incompletely understood. Using affinity purification, mass spectrometry, and phosphopeptide enrichment of isotope-labeled peptides, we examined the dynamic of the CD147 microenvironment and the CD147-dependent phosphoproteome in the Jurkat T cell line upon treatment with T cell stimulating agents. ...[more]

PMID: 28148733

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CD147 mutants affinity purification mass spectrometry from human T cells

Project description:CD147 is known as tumor and regulatory T cell marker and as regulator of chemotaxis, stress response or immune cell function; however, the mode of action of CD147 remains incompletely understood. Using affinity purification mass spectrometry (AP-MS) of HA-tagged CD147 swap and deletion mutants, we examined the CD147 microenvironment. We found previously published interaction partners of CD147 and also identified two highly significant new ones: the plasma membrane calcium ATPase 4 (PMCA4) and moesin. The use of CD147 mutants allowed determining of the respective CD147 parts essential for interaction. Finally, we performed AP-MS of endogenous CD147 from primary human CD4+ T cells and again found CD147 associated with PMCA4.

2016-01-28 | PXD003029 | Pride

CD147 and downstream ADAMTSs promote the tumorigenesis of Kaposi sarcoma-associated herpesvirus

Project description:The Kaposi’s Sarcoma-associated Herpesvirus (KSHV) is the etiologic agent of several human cancers, including Kaposi’s Sarcoma (KS), which preferentially arise in immunocompromised patients but lack of effective therapeutic options. We have previously shown that KSHV or viral protein LANA can upregulate the glycoprotein CD147 (Emmprin) to induce primary endothelial cell invasiveness, which also requires PI3K/Akt and MAPK activation of VEGF production. In the current study, we first time identify the global network controlled by CD147 in KSHV-infected endothelial cells using Illumina microarray analysis. Among these downstream genes, ADAMTS1 and 9, two specific metalloproteases are strongly expressed in AIDS-KS tissues and contributed to KSHV-infected cell invasiveness through regulation of related cytokines production and respective receptors expression. By using a nude mice KS-like model, we found that targeting CD147 and downstream ADAMTSs proteins significantly suppressed KSHV-related tumorigenesis in vivo, which is potentially through impairing extracellular matrix (ECM) formation in tumor microenvironment. Taken together, we think that targeting CD147 and related proteins may represent a promising therapeutic strategy against KSHV-related malignancies.

2016-05-31 | GSE69067 | GEO

CD147 and downstream ADAMTSs promote the tumorigenesis of Kaposi sarcoma-associated herpesvirus

Project description:The Kaposiâs Sarcoma-associated Herpesvirus (KSHV) is the etiologic agent of several human cancers, including Kaposiâs Sarcoma (KS), which preferentially arise in immunocompromised patients but lack of effective therapeutic options. We have previously shown that KSHV or viral protein LANA can upregulate the glycoprotein CD147 (Emmprin) to induce primary endothelial cell invasiveness, which also requires PI3K/Akt and MAPK activation of VEGF production. In the current study, we first time identify the global network controlled by CD147 in KSHV-infected endothelial cells using Illumina microarray analysis. Among these downstream genes, ADAMTS1 and 9, two specific metalloproteases are strongly expressed in AIDS-KS tissues and contributed to KSHV-infected cell invasiveness through regulation of related cytokines production and respective receptors expression. By using a nude mice KS-like model, we found that targeting CD147 and downstream ADAMTSs proteins significantly suppressed KSHV-related tumorigenesis in vivo, which is potentially through impairing extracellular matrix (ECM) formation in tumor microenvironment. Taken together, we think that targeting CD147 and related proteins may represent a promising therapeutic strategy against KSHV-related malignancies. HUVEC cells were infected by KSHV or transduced by a CD147 recombinant adenoviral vector and the gene expression signature was compared to respective controls

2016-05-31 | E-GEOD-69067 | biostudies-arrayexpress

Lateral interactions between B7-H3 and CD147 are essential for stemness in breast cancer: a novel insight from proximal proteome analysis

Project description:Oncogenic cell-surface membrane proteins contribute to the phenotypic and functional characteristics of cancer stem cells (CSCs). We quantitatively analyzed cell-surface membrane proteins that are in close proximity to CD147 in CSCs using proximity-labeling proteomic approach. Moreover, we compared CSCs to non-CSCs to identify CSC-specific cell-surface membrane proteins that are the nearest neighbors of CD147 and revealed that lateral interaction between CD147 and CD276 (B7H3) concealed within the lipid raft microdomain in CSCs confers resistance to docetaxel, known to treat many types of cancer patients including metastatic breast cancer. Furthermore, we found that co-expression of CD147 and CD276 in patients with HER2+ breast cancer who received chemotherapy had poor disease-free survival (DFS) and Overall survival (OS) rates (p = 0.04 and 0.08, respectively). Subsequent immunohistochemical analysis indicated that co-expression of CD147 and CD276 may be associated with poor response to chemotherapy in an independent HER2+ BC cohort. Altogether, our study suggests that the lateral interaction between CD147 and its proximal partners, such as CD276, may be related to a poor prognostic factor in BC and a predictive marker for the critical phenotypic determinant of breast cancer stemness.

2023-10-24 | PXD036909 | Pride

Strength of Neisseria meningitidis binding to endothelial cells requires highly-ordered CD147/β2-adrenoceptor clusters assembled by alpha-actinin-4

Project description:Neisseria meningitidis (meningococcus) is an invasive bacterial pathogen that colonizes human vessels, causing thrombotic lesions and meningitis. Establishment of tight interactions with endothelial cells is crucial for meningococci to resist hemodynamic forces. Two endothelial receptors, CD147 and the β2-adrenergic receptor (β2AR), are sequentially engaged by meningococci to adhere and promote signaling events leading to vascular colonization, but their spatiotemporal coordination is unknown. Here we report that CD147 and β2AR form constitutive hetero-oligomeric complexes. The scaffolding protein alpha-actinin-4 directly binds to the cytosolic tail of CD147 and governs the assembly of CD147/β2AR complexes in highly-ordered clusters at bacterial adhesion sites. This multi-molecular assembly process increases the binding strength of meningococci to endothelial cells under shear stress, and creates molecular platforms for the elongation of membrane protrusions surrounding adherent bacteria. Thus, the specific organization of cellular receptors has major impacts on host-pathogen interaction.

2017-07-10 | PXD006212 | Pride

TAL1 knock down in Jurkat cells

Project description:We used microarray profiling in Jurkat cells to uncover TAL1 dependent genes in a leukemic context.

2010-12-14 | GSE20544 | GEO

TAL1 knock down in Jurkat cells

Project description:We used microarray profiling in Jurkat cells to uncover TAL1 dependent genes in a leukemic context. Clonal Jurkat lines expressing a Doxycycline (Dox) -inducible shRNA against TAL1 coding sequence were generated. A clone in which Dox treatment led to 80% decrease of TAL1 mRNA was chosen.

2010-12-14 | E-GEOD-20544 | biostudies-arrayexpress

Lactate uptake and oxidation via mitochondrial CD147/MCT1/LDHB complex contributes to stemness potentials in metastatic breast cancer

Project description:Metastatic cancer cells, originating from cancer stem cells with metastatic capacity, utilize nutrient flexibility to overcome the hurdles of metastatic cascade. However, the nutrient supply for maintaining the stemness potentials of metastatic cancer cells remains unknown. Here, we revealed that metastatic breast cancer cells maintain stemness and initiate metastasis upon detachment via uptaking and oxidating lactate. In detached metastasizing breast cancer cells, lactate was incorporated into tricarboxylic acid cycle and boosted oxidative phosphorylation, and then promoted the stemness potentials via α-KG-DNMT3B-mediated SOX2 hypomethylation. Moreover, lactate was uptake and oxidated in mitochondria by CD147/MCT1/LDHB complex, whose existence correlates to the stemness potentials and tumor metastasis in breast cancer patients. An intracellularly expressed single chain variable fragment targeting mitochondrial CD147 (mito-CD147 scFv) effectively disrupted mitochondrial CD147/MCT1/LDHB complex, inhibited lactate-induced stemness potentials, depleted circulating breast cancer cells and reduced metastatic burden, suggesting a promising clinical application in reducing lactate-fueled metastasis.

2025-01-09 | PXD059617 |

The adhesin RadD enhances Fusobacterium nucleatum tumor colonization and colorectal carcinogenesis

Project description:Fusobacterium nucleatum can bind to host cells and potentiate intestinal tumorigenesis. Here, we used a genome-wide screen to identify an adhesin, RadD, which facilitates the attachment of F. nucleatum to CRC cells in vitro. RadD directly binds to CD147, a receptor overexpressed on CRC cell surfaces, which initiated a PI3K-AKT-NF-κB-MMP9 cascade, subsequently enhancing tumorigenesis in mice. Clinical specimen analysis showed that elevated radD gene levels in CRC tissues correlated positively with activated oncogenic signaling and poor patient outcomes. Finally, blockade of the interaction between RadD and CD147 in mice effectively impaired F. nucleatum attachment and attenuated F. nucleatum-induced oncogenic response. Together, our study provides insights into an oncogenic mechanism driven by F. nucleatum RadD and suggests that the RadD-CD147 interaction could be a potential therapeutic target for CRC.

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Nucleosome Distribution Data for Methylphenidate Treatment

Project description:Jurkat T-leukemic cells at 0, 15, 45, and 240 minutes post MPH treatment. Chromatin structure depends highly on the position and density of nucleosomes in the genome. The distribution of these nucleosomes likely plays a critical role in all processes for which DNA is the template, including: gene expression, DNA replication, recombination and repair. It has been proposed for more than half a century that although all the cells in a human body contain, essentially, the same genetic material, nucleosomes give access to different areas of the genome effectively giving access to cell-type specific areas of the genome. We hypothesized that alterations in nucleosome distribution might play a role in the MPH stimulated immune response. We measured chromatin structural changes in a human T-cell line (Jurkat T-leukemic) at high temporal resolution after MPH treatment. We mapped the nucleosome distribution at 4 different time points (0, 15, 45, 240 minutes). Nucleosomal DNA sequences were harvested via chromatin cross-linkage, MNase digestion and DNA extraction. Results were gathered by measuring differences in nucleosome distribution between the basal and the treated states at the different time points. We identified changes in nucleosome distribution. Interestingly, these changes in nucleosome distribution were transient, returning to their basal positions. Finally, these changes in nucleosome distribution exhibited different kinetics at different genes. We propose that the changes in nucleosomal distribution help potentiate differences in gene activity. The results allow us to understand the direct affects of MPH on chromatin structure and help reveal certain mechanistic processes by which it performs. Jurkat T-leukemic cells at 0, 15, 45, and 240 minutes post MPH treatment.

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