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Integrin αvβ3 acting as membrane receptor for thyroid hormones mediates angiogenesis in malignant T cells

ABSTRACT: We have found that thyroid hormones (THs), acting as soluble integrin αvβ3 ligands, activate growth-related signaling pathways in T-cell lymphomas (TCL). Specifically, TH-activated αvβ3 integrin signaling promotes TCL proliferation and angiogenesis, in part, via the up-regulation of VEGF.

ORGANISM(S): Homo sapiens

PROVIDER: GSE63122 | GEO | 2015/02/18

SECONDARY ACCESSION(S): PRJNA266733

REPOSITORIES: GEO

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Integrin αvβ3 acting as membrane receptor for thyroid hormones mediates angiogenesis in malignant T cells

Project description:We have found that thyroid hormones (THs), acting as soluble integrin αvβ3 ligands, activate growth-related signaling pathways in T-cell lymphomas (TCL). Specifically, TH-activated αvβ3 integrin signaling promotes TCL proliferation and angiogenesis, in part, via the up-regulation of VEGF. CUTLL1 cells were treated with T3- and T4-bound agarose or agarose alone for 24hrs. Total RNA was harvested from cells and used for expression profiling via RNA-seq.

2015-02-18 | E-GEOD-63122 | biostudies-arrayexpress

MFAP4 is an integrin αVβ3/5 ligand involved in vascular remodeling

Project description:Arterial injury or occlusive arterial disease may stimulate healing responses, which when overexuberant, leads to restenosis of the injured vessel. This response is influenced by specific integrin signalling in vascular smooth muscle cells (VSMCs). Microfibril-associated protein 4 (MFAP4) colocates in blood vessels with elastic fibers. MFAP4 contains an N-terminal RGD-motiv, which is a potential integrin binding site. The role for MFAP4 in vascularproliferative disease is so far unknown and the subject for these investigations. Here we show that MFAP4 is expressed and secreted by VSMCs and binds elastin and collagen. MFAP4 mediated adhesion, and migration, and proliferation of VSMCs in an integrin αVβ3/5 dependent manner and the effects were inhibited by MFAP4 blocking antibodies. MFAP4 deficient mutant mice were generated and appeared with a normal cardiophysiological phenotype. When challenged by carotid artery ligation, the MFAP4 deficient mice had delayed neointimal formation and the compensatory outward remodeling of the vessel diameter and thus the vessel lumen was reduced. MFAP4 expression appeared unaffected by the induced pathology. HUMANE DATA This new MFAP4 mediated molecular mechanism for regulation of integrin αVβ3/5 signalling may have therapeutic implications in diseases where VSMC migration and proliferation are involved in the pathogenesis.

2013-04-01 | GSE40480 | GEO

RhoA GEFs (Lfc subcellular localization and activity is controlled by αv-class integrin)

Project description:Fibronectin (FN)-binding integrins control a variety of cellular responses through Rho GTPases. The FN-binding integrins, αvβ3 and α5β1, are known to induce different effects on cell morphology and motility. Here we report that FN-bound αvβ3 integrin, but not FN-bound α5β1 integrin, triggers the dissociation of the RhoA GEF Lfc (GEF-H1 in humans) from microtubules (MT), leading to the activation of RhoA, formation of stress fibres and maturation of focal adhesions (FAs). Conversely, loss of Lfc expression decreases RhoA activity, stress fibre formation and FA size, suggesting that Lfc is the major GEF downstream of FN-bound αvβ3 that controls RhoA activity. Mechanistically, FN-engaged αvβ3 integrin activates a kinase cascade involving MARK2/3, which in turn leads to phosphorylation of several phospho-sites on Lfc. In particular, S151 was identified as the main site involved in the regulation of Lfc localization and activity. Our findings indicate that activation of Lfc/RhoA is orchestrated in FN-adherent cells in an integrin-specific manner.

2023-04-17 | PXD037596 | Pride

Lfc phospho-proteome (Lfc subcellular localization and activity is controlled by αv-class integrin)

2023-04-17 | PXD037633 | Pride

αvβ3 Integrin Expression and Mitogenic Effects by Thyroid Hormones in Chronic Lymphocytic Leukemia.

Project description: Not available

| S-EPMC8073405 | biostudies-literature

Novel Thyrointegrin αvβ3 antagonist (fp-PMT) with potent affinity in the treatment of cancer

Project description:Microarray analysis was carried out on Glioblastoma (GBM 10181360, GBM 021913 and U87 cells), Bladder cancer (JBV253), skin cancer (A375) and Acute Myelod Leukemia (AML) (KG1A and K562 cells) exposed to fb-PMT at 30 µM concentration. Our genome-wide microarray screens demonstrated that fb-PMT appears to exert its potent anticancer actions on human cancer cells through the molecular interference mechanism with multiple signaling pathways supporting growth and survival of leukemic cells. Notably, fb-PMT had a significant effect on different molecular pathways that contribute to the anticancer activity such as cell cycle control (MYC), survival and maintenance of stem cells (HIF1A; TFAP2C), essential features of the malignant phenotype (TWIST1; SNAI). Furthermore, the fb-PMT-induced significant transcriptional pathway’s activation includes RB1; IRF9; MAML1; RAP1A; and GATA4 pathways, which known to play an important role in anticancer activity. Finally, Consistent with our previous reports on the crosstalk between integrin αvβ3 and ERα which contributes to the induced proliferation of cancer cells, we found that fb-PMT interference with estrogen signaling. The αvβ3 agonist (thyroid hormone) was associated with increased phosphorylation and nuclear enrichment of estrogen receptor α (ERα).

2021-09-11 | GSE183772 | GEO

Loss of the chromatin remodeler, ATRX, promotes aggressive features of osteosarcomas and activates NF-kB signaling and integrin receptor binding

Project description:Osteosarcoma (OS) is a lethal disease with few known targeted therapies. Here we show that decreased ATRX expression is associated with more aggressive tumor cell phenotypes, including increased growth, migration, invasion, and metastasis. These phenotypic changes correspond with activation of NF-κB signaling, extracellular matrix remodeling, increased integrin αvβ3 expression, and ETS family transcription factor binding. However, this increased aggression substantially sensitizes ATRX-deficient OS cells to integrin signaling inhibition. Thus, ATRX plays an important tumor suppression role in OS, and loss of function of this gene may underlie a new therapeutic vulnerability. The relationship of ATRX expression with integrin binding, NF-κB activation, and ETS family transcription factor binding has not been noted in previous studies, but may impact other known diseases with ATRX loss, including other cancers and the ATR-X alpha thalassemia mental retardation syndrome.

2022-10-12 | GSE167546 | GEO

ANTICANCER AGENT P-bi-TAT LINKS THE THYROID HORMONE RECEPTOR ON INTEGRIN αvβ3 TO CANCER CELL METABOLISM/ATP GENERATION.

Project description:ANTICANCER AGENT P-bi-TAT LINKS THE THYROID HORMONE RECEPTOR ON INTEGRIN αvβ3 TO CANCER CELL METABOLISM/ATP GENERATION.

| PRJNA761991 | ENA

ANTICANCER AGENT P-bi-TAT LINKS THE THYROID HORMONE RECEPTOR ON INTEGRIN αvβ3 TO CANCER CELL METABOLISM/ATP GENERATION

Project description:ANTICANCER AGENT P-bi-TAT LINKS THE THYROID HORMONE RECEPTOR ON INTEGRIN αvβ3 TO CANCER CELL METABOLISM/ATP GENERATION

| PRJNA589073 | ENA

Reduced heart failure effects through novel integrin targeting approach

Project description:Heart failure remains one of the largest clinical burdens globally, with little to no improvement in the development of disease-eradicating therapeutics. Integrin targeting has been used in the treatment of ocular disease and cancer, but little is known about its utility in the treatment of heart failure. Here we sought to determine whether the second generation orally available, αvβ3-specific RGD-mimetic, 29P, was cardioprotective. Male mice were subjected to transverse aortic constriction (TAC) and treated with 50μg/kg 29P or volume-matched saline as Vehicle control. At 3 weeks post-TAC, echocardiography showed that 29P treatment significantly restored cardiac function and structure indicating the protective effect of 29P treatment in this model of heart failure. Importantly, 29P treatment improved cardiac function giving improved fractional shortening, ejection fraction, heart weight and lung weight to tibia length fractions, together with partial restoration of Ace and Mme levels, as markers of the TAC insult. At a tissue level, 29P reduced cardiomyocyte hypertrophy and interstitial fibrosis, both of which are major clinical features of heart failure. RNA sequencing identified that, mechanistically, this occurred with concomitant alterations to genes involved molecular pathways associated with these processes such as metabolism, hypertrophy and basement membrane formation. Overall, targeting αvβ3 with 29P provides a novel strategy to attenuate pressure-overload induced cardiac hypertrophy and fibrosis, providing a possible new approach to heart failure treatment.

2024-03-12 | GSE247309 | GEO

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