Comparative proteomic and phosphoproteomic profiling of pancreatic adenocarcinoma cells treated with <scp>CB</scp>1 or <scp>CB</scp>2 agonists

Brandi, Jessica; Dando, Ilaria; Palmieri, Marta; Donadelli, Massimo; Cecconi, Daniela

doi:10.1002/elps.201200402

Cited by 17 publications

(20 citation statements)

References 57 publications

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“…Cannabinoids and their derivatives have recently attracted attention in the treatment of cancer due to their diverse abilities, including anti-inflammation, cell growth inhibition and antitumor properties ( 6 , 10 ). Previous studies have suggested that cannabinoid receptors may be an essential target for the treatment of cancer ( 14 , 15 ). Our previous study indicated that WIN-induced apoptosis of BEL7402 HCC cells may be mediated via the CB2 receptor; therefore, this receptor may be considered as a potential target for the treatment of HCC ( 12 ).…”

Section: Discussionmentioning

confidence: 99%

Cannabinoid WIN55, 212-2 induces cell cycle arrest and inhibits the proliferation and migration of human BEL7402 hepatocellular carcinoma cells

Wang

Zhou

et al. 2015

Molecular Medicine Reports

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Hepatocellular carcinoma (HCC) is the leading cause of cancer-associated mortality worldwide; however, only limited therapeutic treatments are currently available. The present study aimed to investigate the effects of cannabinoids as novel therapeutic targets in HCC. In addition, the mechanism underlying the effects of a synthetic cannabinoid, WIN55, 212-2, on the BEL7402 HCC cell line was investigated. The results demonstrated that WIN55, 212-2 induced cell cycle arrest of the BEL7402 cells at the G0/G1 phase via can nabinoid receptor 2 (CB2)-mediated down regulation of phosphorylated-extracellular signal-regulated kinases (ERK)1/2, upregulation of p27, and downregulation of cyclin D1 and cyclin-dependent kinase 4. Furthermore, inhibition of CB2 with the CB2 antagonist AM630 abrogated WIN55, 212-2-induced cell cycle arrest. Inhibition of ERK1/2 also resulted in cell cycle dysregulation and cell cycle arrest at the G0/G1 phase, which subsequently resulted in cell growth inhibition. In addition, the present study detected a significant reduction in matrix metalloproteinase-9, retinoblastoma protein and E2F1 expression, and migration inhibition by WIN treatment. These results suggested that cannabinoid receptor agonists, including WIN, may be considered as novel therapeutics for the treatment of HCC.

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Section: Discussionmentioning

confidence: 99%

Cannabinoid WIN55, 212-2 induces cell cycle arrest and inhibits the proliferation and migration of human BEL7402 hepatocellular carcinoma cells

Wang

Zhou

et al. 2015

Molecular Medicine Reports

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“…The CB1 and CB2 selective agonists, arachidonylcyclopropylamide (ACPA) and GW, inhibited proliferation and invasion of Panc1 cells, respectively. 55 ACPA and GW through activating the CB1 and CB2 receptors stimulated 5' adenosine monophosphate-activated protein kinase activation via a reactive oxygen species (ROS)-dependent escalate of AMP/ATP ratio, causing cell autophagy and cell growth inhibition. 55,56…”

Section: Resultsmentioning

confidence: 99%

Potential Use of Cannabinoids for the Treatment of Pancreatic Cancer

Sharafi

Nikfarjam

2019

Journal of Pancreatic Cancer

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Background: Cannabinoid extracts may have anticancer properties, which can improve cancer treatment outcomes. The aim of this review is to determine the potentially utility of cannabinoids in the treatment of pancreatic cancer.Methods: A literature review focused on the biological effects of cannabinoids in cancer treatment, with a focus on pancreatic cancer, was conducted. In vitro and in vivo studies that investigated the effects of cannabinoids in pancreatic cancer were identified and potential mechanisms of action were assessed.Results: Cannabinol receptors have been identified in pancreatic cancer with several studies showing in vitro antiproliferative and proapoptotic effects. The main active substances found in cannabis plants are cannabidiol (CBD) and tetrahydrocannabinol (THC). There effects are predominately mediated through, but not limited to cannabinoid receptor-1, cannabinoid receptor-2, and G-protein-coupled receptor 55 pathways. In vitro studies consistently demonstrated tumor growth-inhibiting effects with CBD, THC, and synthetic derivatives. Synergistic treatment effects have been shown in two studies with the combination of CBD/synthetic cannabinoid receptor ligands and chemotherapy in xenograft and genetically modified spontaneous pancreatic cancer models. There are, however, no clinical studies to date showing treatment benefits in patients with pancreatic cancer.Conclusions: Cannabinoids may be an effective adjunct for the treatment of pancreatic cancer. Data on the anticancer effectiveness of various cannabinoid formulations, treatment dosing, precise mode of action, and clinical studies are lacking.

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“…Spots were selected for identification based on significant differences in Student’t t -test ( p < 0.01) and/or good correlations [p(corr) > 0.75] by the multivariate OPLS-DA. Protein identification was performed after in-gel trypsin digestion, as previously described [ 29 ]. Briefly, peptides from each sample were separated by RP nano-HPLC-Chip technology (Agilent Technologies, Palo Alto, CA, USA) online-coupled with a 3D ion trap mass spectrometer (model Esquire 6000, Bruker Daltonics, Bremen, Germany).…”

Section: Methodsmentioning

confidence: 99%

An integrated approach identifies new oncotargets in melanoma

et al. 2017

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Melanoma is an aggressive skin cancer; an early detection of the primary tumor may improve its prognosis. Despite many genes have been shown to be involved in melanoma, the full framework of melanoma transformation has not been completely explored. The characterization of pathways involved in tumor restraint in in vitro models may help to identify oncotarget genes. We therefore aimed to probe novel oncotargets through an integrated approach involving proteomic, gene expression and bioinformatic analysisWe investigated molecular modulations in melanoma cells treated with ascorbic acid, which is known to inhibit cancer growth at high concentrations. For this purpose a proteomic approach was applied. A deeper insight into ascorbic acid anticancer activity was achieved; the discovery of deregulated processes suggested further biomarkers. In addition, we evaluated the expression of identified genes as well as the migration ability in several melanoma cell lines.Data obtained by a multidisciplinary approach demonstrated the involvement of Enolase 1 (ENO1), Parkinsonism-associated deglycase (PARK7), Prostaglansin E synthase 3 (PTGES3), Nucleophosmin (NPM1), Stathmin 1 (STMN1) genes in cell transformation and identified Single stranded DNA binding protein 1 (SSBP1) as a possible onco-suppressor in melanoma cancer.

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Comparative proteomic and phosphoproteomic profiling of pancreatic adenocarcinoma cells treated with CB1 or CB2 agonists

Cited by 17 publications

References 57 publications

Cannabinoid WIN55, 212-2 induces cell cycle arrest and inhibits the proliferation and migration of human BEL7402 hepatocellular carcinoma cells

Cannabinoid WIN55, 212-2 induces cell cycle arrest and inhibits the proliferation and migration of human BEL7402 hepatocellular carcinoma cells

Potential Use of Cannabinoids for the Treatment of Pancreatic Cancer

An integrated approach identifies new oncotargets in melanoma

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