Diversified β-2-adrenergic Receptor Expression and Action in Melanoma Cells

Janik, Marcelina; Szlęzak, Dominika; Surman, Magdalena; Gołas, Aniela; Lityń́ska, Anna; Przybyło, Małgorzata

doi:10.21873/anticanres.11657

Cited by 5 publications

(10 citation statements)

References 35 publications

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“…3-T 1 AM has also been described as an antagonist of muscarinic type 3 receptor (Laurino et al, 2016 ). Furthermore, beta-adrenergic receptors and muscarinic receptors are expressed in multiple melanoma cells including primary uveal melanoma (92.1, Mel202) (Janik et al, 2017 ). In addition, changes in K + channel activity have been implicated in modulating progression of melanoma (Oppitz et al, 2008 ; Luo et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

TRPM8 Activation via 3-Iodothyronamine Blunts VEGF-Induced Transactivation of TRPV1 in Human Uveal Melanoma Cells

et al. 2018

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In human uveal melanoma (UM), tumor enlargement is associated with increases in aqueous humor vascular endothelial growth factor-A (VEGF-A) content that induce neovascularization. 3-Iodothyronamine (3-T1AM), an endogenous thyroid hormone metabolite, activates TRP melastatin 8 (TRPM8), which blunts TRP vanilloid 1 (TRPV1) activation by capsaicin (CAP) in human corneal, conjunctival epithelial cells, and stromal cells. We compare here the effects of TRPM8 activation on VEGF-induced transactivation of TRPV1 in an UM cell line (92.1) with those in normal primary porcine melanocytes (PM) since TRPM8 is upregulated in melanoma. Fluorescence Ca2+-imaging and planar patch-clamping characterized functional channel activities. CAP (20 μM) induced Ca2+ transients and increased whole-cell currents in both the UM cell line and PM whereas TRPM8 agonists, 100 μM menthol and 20 μM icilin, blunted such responses in the UM cells. VEGF (10 ng/ml) elicited Ca2+ transients and augmented whole-cell currents, which were blocked by capsazepine (CPZ; 20 μM) but not by a highly selective TRPM8 blocker, AMTB (20 μM). The VEGF-induced current increases were not augmented by CAP. Both 3-T1AM (1 μM) and menthol (100 μM) increased the whole-cell currents, whereas 20 μM AMTB blocked them. 3-T1AM exposure suppressed both VEGF-induced Ca2+ transients and increases in underlying whole-cell currents. Taken together, functional TRPM8 upregulation in UM 92.1 cells suggests that TRPM8 is a potential drug target for suppressing VEGF induced increases in neovascularization and UM tumor growth since TRPM8 activation blocked VEGF transactivation of TRPV1.

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Section: Discussionmentioning

confidence: 99%

TRPM8 Activation via 3-Iodothyronamine Blunts VEGF-Induced Transactivation of TRPV1 in Human Uveal Melanoma Cells

et al. 2018

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“…In vitro and clinical data suggest a role of adrenaline and noradrenaline, neurotransmitters from the sympathetic NS, in the regulation of melanoma progression 24,27,65 . Thanks to the expression of the adrenergic receptors, human melanoma cells can respond to the catecholamines inside the TME.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, some preclinical studies have demonstrated the role of autonomic NS neurotransmitters such as adrenaline, noradrenaline, aka catecholamines, and acetylcholine in cancer progression 22,23 . Indeed, β1, β2 and β3 catecholamine receptors, physiologically expressed in different tissues and organs, to regulate vital body functions have been also detected in the membrane human melanoma samples and melanoma cell lines 24,25,26 . Activation of β-receptors seem to support cell proliferation, while inducing migration and invasion phenotypes and an EMT-like process in melanoma cells in vitro 24,27 .…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, β1, β2 and β3 catecholamine receptors, physiologically expressed in different tissues and organs, to regulate vital body functions have been also detected in the membrane human melanoma samples and melanoma cell lines 24,25,26 . Activation of β-receptors seem to support cell proliferation, while inducing migration and invasion phenotypes and an EMT-like process in melanoma cells in vitro 24,27 . Recently, a clinicopathological study demonstrated that patients developing a melanoma with high level of β2-receptor expression presented more aggressive and advanced stages of the disease.…”

Section: Introductionmentioning

confidence: 99%

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Melanoma innervation is associated with cancer progression in a zebrafish xenograft model

Lorenzini,

Marines,

Friec

et al. 2023

Preprint

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The peripheral nervous system has a key role in regulating tumour biology in different types of cancer. Here, by modelling aggressive melanoma in larval zebrafish xenografts, we highlight the dynamics of tumour innervation in the tumour microenvironment (TME). Axonogenesis and dendritogenesis are detected in the motoneurons surrounding the melanoma niche and neurogenesis is observed in the nearby population of the enteric nervous system. We also demonstrate the crucial role of catecholamines in promoting melanoma progression, supportingin vivocancer cell dissemination and invasion. Thiszebrafishmodel will allow to uncover neural markers associated with melanoma progression to help in the design of innovative anti-neurogenic therapies targeting specifically the neuronal signals that regulate melanoma progression.Graphical abstractHighlightsTransplantation of human melanoma cells in 3 dpf zebrafish swim bladder allows the development of aggressive melanoma, which cells invade the surrounding organs and migrate over distant locations.The presence of melanoma cells in the larval zebrafish induces morphological changes in the motoneurons inside the tumour niche, including increased axon length and dendritic arborization.The invasion of melanoma cells in the larval intestine promotes neurogenesis of enteric neurons.Transplanted melanoma cells display direct contact with enteric neurons in the intestinal region and migrate along axons to escape from the primary cancer mass, as a mechanism similar to vessel co-option during metastatic dissemination.Catecholamines promote melanoma cell migration and invasion in the zebrafish, modelling melanoma progression.

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“…Alpha (α)-adrenoceptors and beta (β)-adrenoceptors are expressed in both melanoma tissue samples and various melanoma cell lines [ 38 , 56 , 57 , 58 ]. However, adrenergic receptor expression and melanoma cell response to adrenergic stimulation are dependent on both the receptor and the cell type [ 59 ].…”

Section: Neurotransmitters and Melanomamentioning

confidence: 99%

Neuroendocrine Factors in Melanoma Pathogenesis

Scheau

Drăghici

Ilie

et al. 2021

Cancers

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Melanoma is one of the most aggressive skin cancers with a sharp rise in incidence in the last decades, especially in young people. Recognized as a significant public health issue, melanoma is studied with increasing interest as new discoveries in molecular signaling and receptor modulation unlock innovative treatment options. Stress exposure is recognized as an important component in the immune-inflammatory interplay that can alter the progression of melanoma by regulating the release of neuroendocrine factors. Various neurotransmitters, such as catecholamines, glutamate, serotonin, or cannabinoids have also been assessed in experimental studies for their involvement in the biology of melanoma. Alpha-MSH and other neurohormones, as well as neuropeptides including substance P, CGRP, enkephalin, beta-endorphin, and even cellular and molecular agents (mast cells and nitric oxide, respectively), have all been implicated as potential factors in the development, growth, invasion, and dissemination of melanoma in a variety of in vitro and in vivo studies. In this review, we provide an overview of current evidence regarding the intricate effects of neuroendocrine factors in melanoma, including data reported in recent clinical trials, exploring the mechanisms involved, signaling pathways, and the recorded range of effects.

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Diversified β-2-adrenergic Receptor Expression and Action in Melanoma Cells

Abstract: Melanoma cell susceptibility to AD varies depending on origin and progression stage. Metastatic cutaneous melanoma cells were found to be less responsive to AD than primary cutaneous and uveal melanoma cells.

Cited by 5 publications

References 35 publications

TRPM8 Activation via 3-Iodothyronamine Blunts VEGF-Induced Transactivation of TRPV1 in Human Uveal Melanoma Cells

TRPM8 Activation via 3-Iodothyronamine Blunts VEGF-Induced Transactivation of TRPV1 in Human Uveal Melanoma Cells

Melanoma innervation is associated with cancer progression in a zebrafish xenograft model

Neuroendocrine Factors in Melanoma Pathogenesis

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