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Article ; Online: Corrigendum to "The use of cannabinoids as anticancer agents" [Prog. Neuro-Psychopharmacol. Biol. Psychiatry 64 (2016) 259-266].

Velasco, Guillermo / Hernández-Tiedra, Sonia / Dávila, David / Lorente, Mar

Progress in neuro-psychopharmacology & biological psychiatry

2017 Volume 74, Page(s) 57

Language	English
Publishing date	2017--06
Publishing country	England
Document type	Journal Article
ZDB-ID	781181-0
ISSN	1878-4216 ; 0278-5846
ISSN (online)	1878-4216
ISSN	0278-5846
DOI	10.1016/j.pnpbp.2016.12.005
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Article ; Online: The use of cannabinoids as anticancer agents.

Velasco, Guillermo / Hernández-Tiedra, Sonia / Dávila, David / Lorente, Mar

Progress in neuro-psychopharmacology & biological psychiatry

2016 Volume 64, Page(s) 259–266

Abstract: It is well-established that cannabinoids exert palliative effects on some cancer-associated symptoms. In addition evidences obtained during the last fifteen years support that these compounds can reduce tumor growth in animal models of cancer. ... ...

Abstract	It is well-established that cannabinoids exert palliative effects on some cancer-associated symptoms. In addition evidences obtained during the last fifteen years support that these compounds can reduce tumor growth in animal models of cancer. Cannabinoids have been shown to activate an ER-stress related pathway that leads to the stimulation of autophagy-mediated cancer cell death. In addition, cannabinoids inhibit tumor angiogenesis and decrease cancer cell migration. The mechanisms of resistance to cannabinoid anticancer action as well as the possible strategies to develop cannabinoid-based combinational therapies to fight cancer have also started to be explored. In this review we will summarize these observations (that have already helped to set the bases for the development of the first clinical studies to investigate the potential clinical benefit of using cannabinoids in anticancer therapies) and will discuss the possible future avenues of research in this area.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cannabinoids/pharmacology ; Cannabinoids/therapeutic use ; Clinical Trials as Topic ; Endocannabinoids/metabolism ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism
Chemical Substances	Antineoplastic Agents ; Cannabinoids ; Endocannabinoids
Language	English
Publishing date	2016-01-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	781181-0
ISSN	1878-4216 ; 0278-5846
ISSN (online)	1878-4216
ISSN	0278-5846
DOI	10.1016/j.pnpbp.2015.05.010
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Article ; Online: DKWSLLL, a versatile DXXXLL-type signal with distinct roles in the Cu(+)-regulated trafficking of ATP7B.

Lalioti, Vasiliki / Hernandez-Tiedra, Sonia / Sandoval, Ignacio V

Traffic (Copenhagen, Denmark)

2014 Volume 15, Issue 8, Page(s) 839–860

Abstract: In the liver, the P-type ATPase and membrane pump ATP7B plays a crucial role in Cu(+) donation to cuproenzymes and in the elimination of excess Cu(+). ATP7B is endowed with a COOH-cytoplasmic (DE)XXXLL-type traffic signal. We find that accessory (Lys -3, ...

Abstract	In the liver, the P-type ATPase and membrane pump ATP7B plays a crucial role in Cu(+) donation to cuproenzymes and in the elimination of excess Cu(+). ATP7B is endowed with a COOH-cytoplasmic (DE)XXXLL-type traffic signal. We find that accessory (Lys -3, Trp -2, Ser -1 and Leu +2) and canonical (D -4, Leu 0 and Leu +1) residues confer the DKWSLLL signal with the versatility required for the Cu(+)-regulated cycling of ATP7B between the trans-Golgi network (TGN) and the plasma membrane (PM). The separate mutation of these residues caused a disruption of the signal, resulting in different ATP7B distribution phenotypes. These phenotypes indicate the key roles of specific residues at separate steps of ATP7B trafficking, including sorting at the TGN, transport from the TGN to the PM and its endocytosis, and recycling to the TGN and PM. The distinct roles of ATP7B in the TGN and PM and the variety of phenotypes caused by the mutation of the canonical and accessory residues of the DKWSLLL signal can explain the separate or joined presentation of Wilson's cuprotoxicosis and the dysfunction of the cuproenzymes that accept Cu(+) at the TGN.
MeSH term(s)	Adenosine Triphosphatases/chemistry ; Adenosine Triphosphatases/genetics ; Adenosine Triphosphatases/metabolism ; Animals ; COS Cells ; Cation Transport Proteins/chemistry ; Cation Transport Proteins/genetics ; Cation Transport Proteins/metabolism ; Cell Membrane/metabolism ; Cercopithecus aethiops ; Copper/metabolism ; Copper-transporting ATPases ; Hep G2 Cells ; Humans ; Mice ; Protein Sorting Signals ; Protein Transport ; trans-Golgi Network/metabolism
Chemical Substances	Atp7a protein, mouse ; Cation Transport Proteins ; Protein Sorting Signals ; Copper (789U1901C5) ; Adenosine Triphosphatases (EC 3.6.1.-) ; Copper-transporting ATPases (EC 3.6.3.54)
Language	English
Publishing date	2014-06-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1483852-7
ISSN	1600-0854 ; 1398-9219
ISSN (online)	1600-0854
ISSN	1398-9219
DOI	10.1111/tra.12176
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Article ; Online: Human Atg8-cardiolipin interactions in mitophagy: Specific properties of LC3B, GABARAPL2 and GABARAP.

Antón, Zuriñe / Landajuela, Ane / Hervás, Javier H / Montes, L Ruth / Hernández-Tiedra, Sonia / Velasco, Guillermo / Goñi, Felix M / Alonso, Alicia

Autophagy

2016 Volume 12, Issue 12, Page(s) 2386–2403

Abstract: The phospholipid cardiolipin (CL) has been proposed to play a role in selective mitochondrial autophagy, or mitophagy. CL externalization to the outer mitochondrial membrane would act as a signal for the human Atg8 ortholog subfamily, MAP1LC3 (LC3). The ... ...

Abstract	The phospholipid cardiolipin (CL) has been proposed to play a role in selective mitochondrial autophagy, or mitophagy. CL externalization to the outer mitochondrial membrane would act as a signal for the human Atg8 ortholog subfamily, MAP1LC3 (LC3). The latter would mediate both mitochondrial recognition and autophagosome formation, ultimately leading to removal of damaged mitochondria. We have applied quantitative biophysical techniques to the study of CL interaction with various Atg8 human orthologs, namely LC3B, GABARAPL2 and GABARAP. We have found that LC3B interacts preferentially with CL over other di-anionic lipids, that CL-LC3B binding occurs with positive cooperativity, and that the CL-LC3B interaction relies only partially on electrostatic forces. CL-induced increased membrane fluidity appears also as an important factor helping LC3B to bind CL. The LC3B C terminus remains exposed to the hydrophilic environment after protein binding to CL-enriched membranes. In intact U87MG human glioblastoma cells rotenone-induced autophagy leads to LC3B translocation to mitochondria and subsequent delivery of mitochondria to lysosomes. We have also observed that GABARAP, but not GABARAPL2, interacts with CL in vitro. However neither GABARAP nor GABARAPL2 were translocated to mitochondria in rotenone-treated U87MG cells. Thus the various human Atg8 orthologs might play specific roles in different autophagic processes.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Amino Acid Sequence ; Autophagy/drug effects ; Autophagy-Related Protein 8 Family/chemistry ; Autophagy-Related Protein 8 Family/metabolism ; Cardiolipins/metabolism ; Cell Line, Tumor ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Dronabinol/pharmacology ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Hydrophobic and Hydrophilic Interactions ; Microtubule-Associated Proteins/chemistry ; Microtubule-Associated Proteins/metabolism ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondrial Degradation/drug effects ; Mitochondrial Membranes/drug effects ; Mitochondrial Membranes/metabolism ; Pressure ; Protein Binding/drug effects ; Rotenone/pharmacology ; Saccharomyces cerevisiae Proteins/chemistry ; Saccharomyces cerevisiae Proteins/metabolism ; Sequence Homology, Amino Acid
Chemical Substances	ATG8 protein, S cerevisiae ; Adaptor Proteins, Signal Transducing ; Autophagy-Related Protein 8 Family ; Cardiolipins ; GABARAP protein, human ; GABARAPL2 protein, human ; MAP1LC3B protein, human ; Microtubule-Associated Proteins ; Saccharomyces cerevisiae Proteins ; Rotenone (03L9OT429T) ; Dronabinol (7J8897W37S)
Language	English
Publishing date	2016-10-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2016.1240856
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Article ; Online: Optimization of a preclinical therapy of cannabinoids in combination with temozolomide against glioma.

López-Valero, Israel / Torres, Sofía / Salazar-Roa, María / García-Taboada, Elena / Hernández-Tiedra, Sonia / Guzmán, Manuel / Sepúlveda, Juan M / Velasco, Guillermo / Lorente, Mar

Biochemical pharmacology

2018 Volume 157, Page(s) 275–284

Abstract: Glioblastoma multiforme (GBM) is the most frequent and aggressive form of brain cancer. These features are explained at least in part by the high resistance exhibited by these tumors to current anticancer therapies. Thus, the development of novel ... ...

Abstract	Glioblastoma multiforme (GBM) is the most frequent and aggressive form of brain cancer. These features are explained at least in part by the high resistance exhibited by these tumors to current anticancer therapies. Thus, the development of novel therapeutic approaches is urgently needed to improve the survival of the patients suffering this devastating disease. Δ
MeSH term(s)	Administration, Oral ; Animals ; Antineoplastic Combined Chemotherapy Protocols/administration & dosage ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Brain Neoplasms/drug therapy ; Brain Neoplasms/pathology ; Cannabidiol/administration & dosage ; Cannabidiol/therapeutic use ; Carmustine/therapeutic use ; Cell Line, Tumor ; Dronabinol/administration & dosage ; Dronabinol/therapeutic use ; Glioma/drug therapy ; Glioma/pathology ; Heterografts ; Humans ; Male ; Mice, Nude ; Temozolomide/administration & dosage ; Temozolomide/therapeutic use
Chemical Substances	Cannabidiol (19GBJ60SN5) ; Dronabinol (7J8897W37S) ; Carmustine (U68WG3173Y) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2018-08-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2018.08.023
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Article ; Online: Midkine signaling maintains the self-renewal and tumorigenic capacity of glioma initiating cells.

López-Valero, Israel / Dávila, David / González-Martínez, José / Salvador-Tormo, Nélida / Lorente, Mar / Saiz-Ladera, Cristina / Torres, Sofía / Gabicagogeascoa, Estibaliz / Hernández-Tiedra, Sonia / García-Taboada, Elena / Mendiburu-Eliçabe, Marina / Rodríguez-Fornés, Fátima / Sánchez-Domínguez, Rebeca / Segovia, José Carlos / Sánchez-Gómez, Pilar / Matheu, Ander / Sepúlveda, Juan M / Velasco, Guillermo

Theranostics

2020 Volume 10, Issue 11, Page(s) 5120–5136

Abstract: Glioblastoma (GBM) is one of the most aggressive forms of cancer. It has been proposed that the presence within these tumors of a population of cells with stem-like features termed Glioma Initiating Cells (GICs) is responsible for the relapses that take ... ...

Abstract	Glioblastoma (GBM) is one of the most aggressive forms of cancer. It has been proposed that the presence within these tumors of a population of cells with stem-like features termed Glioma Initiating Cells (GICs) is responsible for the relapses that take place in the patients with this disease. Targeting this cell population is therefore an issue of great therapeutic interest in neuro-oncology. We had previously found that the neurotrophic factor MIDKINE (MDK) promotes resistance to glioma cell death. The main objective of this work is therefore investigating the role of MDK in the regulation of GICs.
MeSH term(s)	Anaplastic Lymphoma Kinase/antagonists & inhibitors ; Anaplastic Lymphoma Kinase/metabolism ; Animals ; Antineoplastic Agents, Alkylating/pharmacology ; Autophagy/drug effects ; Brain Neoplasms/drug therapy ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Cell Line ; Female ; Glioma/drug therapy ; Glioma/metabolism ; Glioma/pathology ; Humans ; Mice ; Mice, Nude ; Midkine/antagonists & inhibitors ; Midkine/metabolism ; Neoplastic Stem Cells/metabolism ; Signal Transduction ; Temozolomide/pharmacology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents, Alkylating ; MDK protein, human ; Midkine (137497-38-2) ; ALK protein, human (EC 2.7.10.1) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2020-04-06
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.41450
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Article ; Online: Detecting autophagy in response to ER stress signals in cancer.

Salazar, María / Hernández-Tiedra, Sonia / Torres, Sofía / Lorente, Mar / Guzmán, Manuel / Velasco, Guillermo

Methods in enzymology

2011 Volume 489, Page(s) 297–317

Abstract: Different physiological and pathological situations that produce alterations in the endoplasmic reticulum, lead to a condition known as ER stress. ER stress activates a complex intracellular signal transduction pathway, called unfolded protein response ( ... ...

Abstract	Different physiological and pathological situations that produce alterations in the endoplasmic reticulum, lead to a condition known as ER stress. ER stress activates a complex intracellular signal transduction pathway, called unfolded protein response (UPR). UPR is tailored essentially to reestablish ER homeostasis. However, when persistent, ER stress can switch the cytoprotective functions of UPR into cell death promoting mechanisms. One of the cellular mechanisms that are regulated by ER stress is autophagy. Autophagy is a cellular process by which different cytoplasmic components including organelles are targeted for degradation to the autophagosomes. Interestingly, like ER stress, autophagy can be a protective or a cell death promoting mechanism. Recently, a variety of anticancer therapies (including those that stimulate ER stress) have been shown to activate autophagy in tumor cells, which has been proposed to either enhance cancer cell death or act as a mechanism of resistance to chemotherapy. In this chapter, we will describe some of the procedures that are currently used to analyze autophagy as well as some of the experimental approaches that can be undertaken to investigate the connection between ER stress and autophagy in cancer.
MeSH term(s)	Animals ; Autophagy/physiology ; Cells, Cultured ; Endoplasmic Reticulum/pathology ; Endoplasmic Reticulum/physiology ; Fluorescent Antibody Technique ; Humans ; Mechanistic Target of Rapamycin Complex 1 ; Microtubule-Associated Proteins/physiology ; Multiprotein Complexes ; Neoplasm Transplantation ; Neoplasms/pathology ; Proteins/metabolism ; RNA Interference ; Signal Transduction/physiology ; Stress, Physiological ; TOR Serine-Threonine Kinases ; Transplantation, Heterologous ; Unfolded Protein Response
Chemical Substances	MAP1LC3A protein, human ; Microtubule-Associated Proteins ; Multiprotein Complexes ; Proteins ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2011-01-13
Publishing country	United States
Document type	Journal Article
ISSN	1557-7988
ISSN (online)	1557-7988
DOI	10.1016/B978-0-12-385116-1.00017-0
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Article ; Online: Targeting Glioma Initiating Cells with A combined therapy of cannabinoids and temozolomide.

López-Valero, Israel / Saiz-Ladera, Cristina / Torres, Sofía / Hernández-Tiedra, Sonia / García-Taboada, Elena / Rodríguez-Fornés, Fátima / Barba, Marina / Dávila, David / Salvador-Tormo, Nélida / Guzmán, Manuel / Sepúlveda, Juan M / Sánchez-Gómez, Pilar / Lorente, Mar / Velasco, Guillermo

Biochemical pharmacology

2018 Volume 157, Page(s) 266–274

Abstract: Glioblastoma multiforme (GBM) is the most frequent and aggressive type of brain tumor due, at least in part, to its poor response to current anticancer treatments. These features could be explained, at least partially, by the presence within the tumor ... ...

Abstract	Glioblastoma multiforme (GBM) is the most frequent and aggressive type of brain tumor due, at least in part, to its poor response to current anticancer treatments. These features could be explained, at least partially, by the presence within the tumor mass of a small population of cells termed Glioma Initiating Cells (GICs) that has been proposed to be responsible for the relapses occurring in this disease. Thus, the development of novel therapeutic approaches (and specifically those targeting the population of GICs) is urgently needed to improve the survival of the patients suffering this devastating disease. Previous observations by our group and others have shown that Δ
MeSH term(s)	Animals ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Brain Neoplasms/drug therapy ; Brain Neoplasms/pathology ; Cannabidiol/therapeutic use ; Cell Line, Tumor ; Dronabinol/therapeutic use ; Female ; Glioblastoma/drug therapy ; Glioblastoma/pathology ; Humans ; Male ; Mice, Nude ; Neoplastic Stem Cells/drug effects ; Temozolomide/therapeutic use ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Cannabidiol (19GBJ60SN5) ; Dronabinol (7J8897W37S) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2018-09-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2018.09.007
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Article ; Online: Daxx functions as a scaffold of a protein assembly constituted by GLUT4, JNK1 and KIF5B.

Lalioti, Vasiliki S / Vergarajauregui, Silvia / Tsuchiya, Yo / Hernandez-Tiedra, Sonia / Sandoval, Ignacio V

Journal of cellular physiology

2009 Volume 218, Issue 2, Page(s) 416–426

Abstract: We have previously reported the physical interaction between Daxx, the adaptor protein that mediates activation of the Jun amino-terminal kinase (JNK), and GLUT4, the insulin-dependent glucose transporter, interaction that involves their C-domains. Co- ... ...

Abstract	We have previously reported the physical interaction between Daxx, the adaptor protein that mediates activation of the Jun amino-terminal kinase (JNK), and GLUT4, the insulin-dependent glucose transporter, interaction that involves their C-domains. Co-immunoprecipitation and two-hybrid-based protein-protein interaction studies show now that Daxx and GLUT4 interact with JNK1 through D-sites in their NH(2)-(aa 1-501) and large endofacial loop, respectively. Serum deprivation strongly enhances the association of JNK1 with Daxx and dissociates the kinase from GLUT4. SP600125, a potent JNK1 inhibitor, reduces the JNK1 activity associated with GLUT4 and the phosphorylation of two minor GLUT4 species in serum-starved 3T3-L1 adipocytes. In addition, Daxx interacts with kinesin KIF5B through the 6xTPR domain of the kinesin light chain, a domain engaged in the grab hold of protein cargo by kinesin motors that codistribute with JNK. Depletion of Daxx in 3T3-L1 adipocytes provokes the partial translocation of the GLUT4 retained in the GLUT4 storage compartment to endosomes.
MeSH term(s)	3T3-L1 Cells ; Adipocytes/drug effects ; Adipocytes/enzymology ; Animals ; Anthracenes/pharmacology ; Carrier Proteins/chemistry ; Carrier Proteins/metabolism ; Glucose Transporter Type 4/chemistry ; Glucose Transporter Type 4/metabolism ; Humans ; Immunoprecipitation ; Insulin Receptor Substrate Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/chemistry ; Intracellular Signaling Peptides and Proteins/metabolism ; Kinesin/metabolism ; Mice ; Microtubules/drug effects ; Microtubules/metabolism ; Mitogen-Activated Protein Kinase 8/antagonists & inhibitors ; Mitogen-Activated Protein Kinase 8/chemistry ; Mitogen-Activated Protein Kinase 8/metabolism ; Nuclear Proteins/chemistry ; Nuclear Proteins/metabolism ; Phosphorylation/drug effects ; Protein Binding/drug effects ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Transport/drug effects ; Rats ; Serum
Chemical Substances	Anthracenes ; Carrier Proteins ; Daxx protein, mouse ; Glucose Transporter Type 4 ; Insulin Receptor Substrate Proteins ; Intracellular Signaling Peptides and Proteins ; Irs1 protein, mouse ; Nuclear Proteins ; pyrazolanthrone (1TW30Y2766) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24) ; Kif5b protein, mouse (EC 3.6.1.-) ; Kinesin (EC 3.6.4.4)
Language	English
Publishing date	2009-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.21614
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Article ; Online: Exploiting cannabinoid-induced cytotoxic autophagy to drive melanoma cell death.

Armstrong, Jane L / Hill, David S / McKee, Christopher S / Hernandez-Tiedra, Sonia / Lorente, Mar / Lopez-Valero, Israel / Eleni Anagnostou, Maria / Babatunde, Fiyinfoluwa / Corazzari, Marco / Redfern, Christopher P F / Velasco, Guillermo / Lovat, Penny E

The Journal of investigative dermatology

2015 Volume 135, Issue 6, Page(s) 1629–1637

Abstract: Although the global incidence of cutaneous melanoma is increasing, survival rates for patients with metastatic disease remain <10%. Novel treatment strategies are therefore urgently required, particularly for patients bearing BRAF/NRAS wild-type tumors. ... ...

Abstract	Although the global incidence of cutaneous melanoma is increasing, survival rates for patients with metastatic disease remain <10%. Novel treatment strategies are therefore urgently required, particularly for patients bearing BRAF/NRAS wild-type tumors. Targeting autophagy is a means to promote cancer cell death in chemotherapy-resistant tumors, and the aim of this study was to test the hypothesis that cannabinoids promote autophagy-dependent apoptosis in melanoma. Treatment with Δ(9)-Tetrahydrocannabinol (THC) resulted in the activation of autophagy, loss of cell viability, and activation of apoptosis, whereas cotreatment with chloroquine or knockdown of Atg7, but not Beclin-1 or Ambra1, prevented THC-induced autophagy and cell death in vitro. Administration of Sativex-like (a laboratory preparation comprising equal amounts of THC and cannabidiol (CBD)) to mice bearing BRAF wild-type melanoma xenografts substantially inhibited melanoma viability, proliferation, and tumor growth paralleled by an increase in autophagy and apoptosis compared with standard single-agent temozolomide. Collectively, our findings suggest that THC activates noncanonical autophagy-mediated apoptosis of melanoma cells, suggesting that cytotoxic autophagy induction with Sativex warrants clinical evaluation for metastatic disease.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins/metabolism ; Autophagy ; Beclin-1 ; Cannabidiol ; Cannabinoids/chemistry ; Cannabinol/chemistry ; Cell Death ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Dacarbazine/analogs & derivatives ; Dacarbazine/chemistry ; Dronabinol/chemistry ; Drug Combinations ; Humans ; Male ; Melanoma/metabolism ; Melanoma/pathology ; Membrane Proteins/metabolism ; Mice ; Mice, Nude ; Microscopy, Confocal ; Neoplasm Metastasis ; Neoplasm Transplantation ; Neoplasms/metabolism ; Plant Extracts/chemistry ; Proto-Oncogene Proteins B-raf/metabolism ; Skin Neoplasms/metabolism ; Temozolomide ; ras Proteins/metabolism
Chemical Substances	AMBRA1 protein, human ; Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; BECN1 protein, human ; Beclin-1 ; Cannabinoids ; Drug Combinations ; Membrane Proteins ; Plant Extracts ; Cannabidiol (19GBJ60SN5) ; Dacarbazine (7GR28W0FJI) ; Dronabinol (7J8897W37S) ; Cannabinol (7UYP6MC9GH) ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; ras Proteins (EC 3.6.5.2) ; nabiximols (K4H93P747O) ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2015-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1038/jid.2015.45
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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