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MCPIP2 competes with IGF2BP1 binding to common stem-loop structure in the 3’UTRs of pro-angiogenic genes for suppressing breast tumor angiogenesis

ABSTRACT: This study was performed according to protein pull-down assay using GFP-coated beads in GFP-MCPIP2 fusion protein expressed MDA-MB-468 cells, and then the pulled down proteins were isolated by running SDS-PAGE and silver staining, and identified by high resolution mass spectrometry.

ORGANISM(S): Homo Sapiens

SUBMITTER: Wenbao Lu

PROVIDER: PXD052919 | iProX | Wed Jun 05 00:00:00 GMT+01:00 2024

REPOSITORIES: iProX

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The RNA-Binding Proteins MCPIP2 and IGF2BP1 Competitively Modulate Breast Tumor Angiogenesis by Antagonizing VEGFA mRNA Stability and Expression.

Lu Wenbao W Li Hongwei H Liu Xueting X Li Ailing A Xiu Ruijuan R

FASEB journal : official publication of the Federation of American Societies for Experimental Biology 20250501 10

Tumor angiogenesis is essential for further growth and metastasis of solid tumors. However, the mechanisms underlying angiogenesis-related gene expression have yet to be clarified. Here, we discovered RNA-binding proteins monocyte chemotactic protein-induced protein 2 (MCPIP2) and insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) function as a pair of antagonists that modulate breast tumor angiogenesis by competitively regulating mRNA stability of proangiogenic gene transcripts, incl ...[more]

PMID: 40354028

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MCPIP2 competes with IGF2BP1 binding to common stem-loop structure in the 3’UTRs of pro-angiogenic genes for suppressing breast tumor angiogenesis-2

Project description:This study was performed according to RNA pull-down assay using biotin-labeled WT RNA probe (with stem-loop structure) or mutant RNA probe (without stem-loop structure) and streptavidin-coated Dynabeads in human breast tumor cell MDA-MB-468, and then the pulled down proteins were isolated by SDS-PAGE and silver staining, and identified by high resolution mass spectrometry.

2024-06-05 | PXD052920 |

DDX5 competes with ZC3H12D regulating CCND1 transcript stability to modulate cell cycle progression in breast cancer

Project description:This study was performed according to protein pull-down assay using GFP-coated beads in MDA-MB-468 cells expressing GFP/ZC3H12D fusion protein, and then the precipitated proteins were isolated by running SDS-PAGE and silver staining, and identified by high resolution mass spectrometry.This study was performed according to RNA pull-down assay using biotin-labeled WT RNA probe (with stem-loop structure) or mutant RNA probe (without stem-loop structure) and streptavidin-coated Dynabeads in human breast tumor cell MDA-MB-468, and then the pulled down proteins were isolated by SDS-PAGE and silver staining, and identified by high resolution mass spectrometry.

2024-10-21 | PXD057000 |

Common polymorphisms in angiogenesis.

Project description:A wide variety of diseases have a significant genetic component, including major causes of morbidity and mortality in the western world. Many of these diseases are also angiogenesis dependent. In humans, common polymorphisms, although more subtle in effect than rare mutations that cause Mendelian disease, are expected to have greater overall effects on human disease. Thus, common polymorphisms in angiogenesis-regulating genes may affect the response to an angiogenic stimulus and thereby affect susceptibility to or progression of such diseases. Candidate gene studies have identified several associations between angiogenesis gene polymorphisms and disease. Similarly, emerging pharmacogenomic evidence indicates that several angiogenesis-regulating polymorphisms may predict response to therapy. In contrast, genome-wide association studies have identified only a few risk alleles in obvious angiogenesis genes. As in other traits, regulatory polymorphisms appear to dominate the landscape of angiogenic responsiveness. Rodent assays, including the mouse corneal micropocket assay, tumor models, and a macular degeneration model have allowed the identification and comparison of loci that directly affect the trait. Complementarity between human and animal approaches will allow increased understanding of the genetic basis for angiogenesis-dependent disease.

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Common Tumor Suppressive Signaling of Thyroid Hormone Receptor Beta in Breast and Thyroid Cancer Cells

Project description:The thyroid hormone receptor beta (TRβ) is a tumor suppressor in multiple types of solid tumors, most prominently in breast and thyroid cancer. An increased understanding of the molecular mechanisms by which TRβ abrogates tumorigenesis could aid in understanding the core tumor suppressive program that TRβ facilitates. Here, we introduce TRβ into the MDA-MB-468 basal-like breast cancer cell line and perform RNA-sequencing to determine changes in transcriptomic signaling. The TRβ expressing MDA-MB-468 cells exhibit a more epithelial character as determined by PCA-PAM50 score and through repression of mesenchymal cytokeratins. The epithelial to mesenchymal transition pathway is also significantly reduced. The MDA-MB-468 dataset was also compared to RNA sequencing results from the thyroid cancer line SW1736 to determine which genes are TRβ regulated across both tissue types. Stearate biosynthesis was revealed as upregulated from the shared gene set, a lipid which is known to repress breast tumorigenesis, as were chromatin remodeling pathways. These data provide novel insights into the molecular mechanisms by which TRβ suppresses breast tumorigenesis and suggests a common metabolic role in breast and thyroid cancer as well a role for TRβ in the maintenance of epithelial cellular identity.

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? Opioids inhibit tumor angiogenesis by suppressing VEGF signaling.

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Pro-Calcific Environment Impairs Ischaemia-Driven Angiogenesis.

Project description:Peripheral arterial disease (PAD) is characterised by accelerated arterial calcification and impairment in angiogenesis. Studies implicate vascular calcification as a contributor to PAD, but the mechanisms remain unclear. We aimed to determine the effect of calcification on ischaemia-driven angiogenesis. Human coronary artery endothelial cells (ECs) were treated with calcification medium (CM: CaCl2 2.7 mM, Na2PO4 2.0 mM) for 24 h and exposed to normoxia (5% CO2) or hypoxia (1.2% O2; 5% CO2 balanced with N2). In normoxia, CM significantly inhibited tubule formation and migration and upregulated calcification markers of ALP, BMP2, and Runx2. CM elevated levels of calcification-protective gene OPG, demonstrating a compensatory mechanism by ECs. CM failed to induce pro-angiogenic regulators VEGFA and HIF-1α in hypoxia and further suppressed the phosphorylation of endothelial nitric oxide synthase (eNOS) that is essential for vascular function. In vivo, osteoprotegerin-deficient mice (OPG-/-), a calcification model, were subjected to hind-limb ischaemia (HLI) surgery. OPG-/- mice displayed elevated serum alkaline phosphatase (ALP) activity compared to wild-type controls. OPG-/- mice experienced striking reductions in blood-flow reperfusion in both 8-week-old and 6-month-old mice post-HLI. This coincided with significant impairment in tissue ischaemia and reduced limb function as assessed by clinical scoring (Tarlov). This study demonstrated for the first time that a pro-calcific environment is detrimental to ischaemia-driven angiogenesis. The degree of calcification in patients with PAD can often be a limiting factor with the use of standard therapies. These highly novel findings require further studies for full elucidation of the mechanisms involved and have implications for the development of therapies to suppress calcification in PAD.

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Apigenin inhibits tumor angiogenesis by suppressing microvesicle biogenesis

Project description:Apigenin regulates multiple pathways related to microvesicle biogenesis without affecting the expression of small Rho GTPase activator guanine nucleotide exchange factors (GEFs). However, apigenin can primarily targets ARHGEF1 protein, a GEF of the small GTPases, thereby inhibiting the activity of small G proteins such as Cdc42, which is essential in regulating the signaling for the release of microvesicles from tumor cells. Targeting ARHGEF1, apigenin effectively prevents tumor cells from releasing microvesicles. This, in turn, inhibits tumor angiogenesis related to VEGF90K transport on microvesicles, ultimately impeding tumor progression.

2024-07-22 | GSE251817 | GEO

Identification of FLS2 interacting proteins by co-immunoprecipitation and shot gun proteomics

Project description:To identify immediate early signaling components in the FLS2 pathway we performed co-immunoprecipitation (co-IP) experiments with FLS2-GFP as bait in Arabidopsis. We immunoprecipitated FLS2-GFP with anti-GFP antibody coated beads and analyzed co-precipitated proteins by liquid chromatography tandem mass spectrometry (LC-MS/MS).

2016-01-26 | PXD003189 | Pride

Chromatin accessibility analysis uncovers TFAP2A as a regulator on pro-angiogenesis of acquired resistance to anlotinib

Project description:Anlotinib, a multitarget agent a multi-target agent that inhibits tumor proliferation and angiogenesis, has been demonstrated to be effective for non-small cell lung cancer (NSCLC) at third-line or over third-line. However, the underlying mechanisms of anlotinib acquired-resistance is still unclear. Here we performed chromatin accessibility profiling on anlotinib-resistant NCI-H1975 and wild-type NCI-H1975. By integrating with transcriptome analysis, we found that anlotinib resistance was due to increased angiogenic capacity, and revealed that TFAP2A was involved in anlotinib resistance. Next, TFAP2A was knock-down in anlotinib-resistant cells and RNAseq was performed to see down-regulated genes with TFAP2A KD.

2020-11-09 | GSE142031 | GEO

A pro-inflammatory signature mediates FGF2-induced angiogenesis.

Project description:Fibroblast growth factor-2 (FGF2) is a potent angiogenic growth factor. Here, gene expression profiling of FGF2-stimulated microvascular endothelial cells revealed, together with a prominent pro-angiogenic profile, a pro-inflammatory signature characterized by the upregulation of pro-inflammatory cytokine/chemokines and their receptors, endothelial cell adhesion molecules and members of the eicosanoid pathway. Real-time quantitative PCR demonstrated early induction of most of the FGF2-induced, inflammation-related genes. Accordingly, chick embryo chorioallantoic membrane (CAM) and murine Matrigel plug angiogenesis assays demonstrated a significant monocyte/macrophage infiltrate in the areas of FGF2-driven neovascularization. Similar results were obtained when the conditioned medium (CM) of FGF2-stimulated endothelial cells was delivered onto the CAM, suggesting that FGF2-upregulated chemoattractants mediate the inflammatory response. Importantly, FGF2-triggered new blood vessel formation was significantly reduced in phosphatidylinositol 3-kinase-gamma null mice exhibiting defective leucocyte migration or in clodronate liposome-treated, macrophage-depleted mice. Furthermore, the viral pan-chemokine antagonist M3 inhibited the angiogenic and inflammatory responses induced by the CM of FGF2-stimulated endothelial cells and impaired FGF2-driven neovascularization in the CAM assay. These findings point to inflammatory chemokines as early mediators of FGF2-driven angiogenesis and indicate a non-redundant role for inflammatory cells in the neovascularization process elicited by the growth factor.

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