Anticancer activity of anandamide in human cutaneous melanoma cells

Adinolfi, Barbara; Romanini, Antonella; Vanni, A.; Martinotti, Enrica; Chicca, Andrea; Fogli, Stefano; Nieri, Paola

doi:10.1016/j.ejphar.2013.08.039

Cited by 65 publications

(71 citation statements)

References 32 publications

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“…In addition, GPR55 is expressed in malignant tumors as well including cholangiocarcinoma cells, melanoma cells or human squamous cell carcinomas. The role of GPR55 activation seems to be cell type specific: while in cholangiocarcinoma cells and melanoma cells activation of GPR55 has anti-proliferative or even toxic effects [35,36] in human squamous cell carcinomas drives skin carcinogenesis [37]. …”

Section: Resultsmentioning

confidence: 99%

CB2 Receptor Activation Inhibits Melanoma Cell Transmigration through the Blood-Brain Barrier

Haskó

Fazakas

Molnár

et al. 2014

IJMS

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During parenchymal brain metastasis formation tumor cells need to migrate through cerebral endothelial cells, which form the morphological basis of the blood-brain barrier (BBB). The mechanisms of extravasation of tumor cells are highly uncharacterized, but in some aspects recapitulate the diapedesis of leukocytes. Extravasation of leukocytes through the BBB is decreased by the activation of type 2 cannabinoid receptors (CB2); therefore, in the present study we sought to investigate the role of CB2 receptors in the interaction of melanoma cells with the brain endothelium. First, we identified the presence of CB1, CB2(A), GPR18 (transcriptional variant 1) and GPR55 receptors in brain endothelial cells, while melanoma cells expressed CB1, CB2(A), GPR18 (transcriptional variants 1 and 2), GPR55 and GPR119. We observed that activation of CB2 receptors with JWH-133 reduced the adhesion of melanoma cells to the layer of brain endothelial cells. JWH-133 decreased the transendothelial migration rate of melanoma cells as well. Our results suggest that changes induced in endothelial cells are critical in the mediation of the effect of CB2 agonists. Our data identify CB2 as a potential target in reducing the number of brain metastastes originating from melanoma.

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Section: Resultsmentioning

confidence: 99%

CB2 Receptor Activation Inhibits Melanoma Cell Transmigration through the Blood-Brain Barrier

Haskó

Fazakas

Molnár

et al. 2014

IJMS

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“…These include a variety of peripheral and central inflammatory states as well as certain forms of cancer. [23, 73] The wide potential applicability of these agents provides a great therapeutic opportunity, but also poses interesting challenges to medicinal chemistry. In addition to balanced potency for FAAH and COX, future molecules should be able to engage these proteins in all compartments of the body, including the central nervous system, and to selectively target FAAH/COX-1 versus FAAH/COX-2.…”

Section: Future Perspectivesmentioning

confidence: 99%

A Double Whammy: Targeting Both Fatty Acid Amide Hydrolase (FAAH) and Cyclooxygenase (COX) To Treat Pain and Inflammation

Sasso

Piomelli

2015

ChemMedChem

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Pain states that arise from non-resolving inflammation, such as inflammatory bowel disease or arthritis, pose an unusually difficult challenge for therapy because of the complexity and heterogeneity of their underlying mechanisms. It has been suggested that key nodes linking interactive pathogenic pathways of non-resolving inflammation might offer novel targets for the treatment of inflammatory pain. Non-steroidal anti-inflammatory drugs (NSAIDs), which inhibit the cyclooxygenase (COX)-mediated production of pain- and inflammation-inducing prostanoids, are a common first-line treatment for this condition, but their use is limited by mechanism-based side effects. The endogenous levels of anandamide, an endocannabinoid mediator with analgesic and tissue protective functions, are regulated by fatty acid amide hydrolase (FAAH). The present article outlines the pharmacological and chemical rationale for the simultaneous inhibition of COX and FAAH activities with designed multi-target agents. Preclinical studies indicate that such agents may combine superior anti-inflammatory efficacy with reduced toxicity.

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“…Increasing evidence supports that GPR55 is an important component of the molecular circuitry that controls cancer cell behavior. Thus, this receptor has been shown to drive cancer cell proliferation in in vitro and/or in vivo models of glioblastoma [10]; prostate [11], ovarian [11] and skin carcinoma [12]; melanoma [13], and non-small lung cancer [14]. GPR55 has also been indirectly associated to both pro-angiogenic responses [15] and to pro-migratory phenotypes in breast [16] and colon cancer cells [17].…”

Section: Introductionmentioning

confidence: 99%

Activation of the orphan receptor GPR55 by lysophosphatidylinositol promotes metastasis in triple-negative breast cancer

et al. 2016

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The orphan G protein-coupled receptor GPR55 has been directly or indirectly related to basic alterations that drive malignant growth: uncontrolled cancer cell proliferation, sustained angiogenesis, and cancer cell adhesion and migration. However, little is known about the involvement of this receptor in metastasis. Here, we show that elevated GPR55 expression in human tumors is associated with the aggressive basal/triple-negative breast cancer population, higher probability to develop metastases, and therefore poor patient prognosis. Activation of GPR55 by its proposed endogenous ligand lysophosphatidylinositol confers pro-invasive features on breast cancer cells both in vitro and in vivo. Specifically, this effect is elicited by coupling to Gq/11 heterotrimeric proteins and the subsequent activation, through ERK, of the transcription factor ETV4/PEA3. Together, these data show that GPR55 promotes breast cancer metastasis, and supports the notion that this orphan receptor may constitute a new therapeutic target and potential biomarker in the highly aggressive triple-negative subtype.

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Anticancer activity of anandamide in human cutaneous melanoma cells

Cited by 65 publications

References 32 publications

CB2 Receptor Activation Inhibits Melanoma Cell Transmigration through the Blood-Brain Barrier

CB2 Receptor Activation Inhibits Melanoma Cell Transmigration through the Blood-Brain Barrier

A Double Whammy: Targeting Both Fatty Acid Amide Hydrolase (FAAH) and Cyclooxygenase (COX) To Treat Pain and Inflammation

Activation of the orphan receptor GPR55 by lysophosphatidylinositol promotes metastasis in triple-negative breast cancer

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