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Article ; Online: Cancer cell autophagy, reprogrammed macrophages, and remodeled vasculature in glioblastoma triggers tumor immunity.

Chryplewicz, Agnieszka / Scotton, Julie / Tichet, Mélanie / Zomer, Anoek / Shchors, Ksenya / Joyce, Johanna A / Homicsko, Krisztian / Hanahan, Douglas

Cancer cell

2022 Volume 40, Issue 10, Page(s) 1111–1127.e9

Abstract: Glioblastoma (GBM) is poorly responsive to therapy and invariably lethal. One conceivable strategy to circumvent this intractability is to co-target distinctive mechanistic components of the disease, aiming to concomitantly disrupt multiple capabilities ... ...

Abstract	Glioblastoma (GBM) is poorly responsive to therapy and invariably lethal. One conceivable strategy to circumvent this intractability is to co-target distinctive mechanistic components of the disease, aiming to concomitantly disrupt multiple capabilities required for tumor progression and therapeutic resistance. We assessed this concept by combining vascular endothelial growth factor (VEGF) pathway inhibitors that remodel the tumor vasculature with the tricyclic antidepressant imipramine, which enhances autophagy in GBM cancer cells and unexpectedly reprograms immunosuppressive tumor-associated macrophages via inhibition of histamine receptor signaling to become immunostimulatory. While neither drug is efficacious as monotherapy, the combination of imipramine with VEGF pathway inhibitors orchestrates the infiltration and activation of CD8 and CD4 T cells, producing significant therapeutic benefit in several GBM mouse models. Inclusion up front of immune-checkpoint blockade with anti-programmed death-ligand 1 (PD-L1) in eventually relapsing tumors markedly extends survival benefit. The results illustrate the potential of mechanism-guided therapeutic co-targeting of disparate biological vulnerabilities in the tumor microenvironment.
MeSH term(s)	Animals ; Antidepressive Agents, Tricyclic/metabolism ; Antidepressive Agents, Tricyclic/therapeutic use ; Autophagy ; B7-H1 Antigen/metabolism ; Glioblastoma/pathology ; Imipramine/metabolism ; Imipramine/therapeutic use ; Immune Checkpoint Inhibitors ; Immunotherapy ; Macrophages/metabolism ; Mice ; Neoplasm Recurrence, Local/drug therapy ; Programmed Cell Death 1 Receptor ; Tumor Microenvironment ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Antidepressive Agents, Tricyclic ; B7-H1 Antigen ; Immune Checkpoint Inhibitors ; Programmed Cell Death 1 Receptor ; Vascular Endothelial Growth Factor A ; Imipramine (OGG85SX4E4)
Language	English
Publishing date	2022-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2022.08.014
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Bispecific PD1-IL2v and anti-PD-L1 break tumor immunity resistance by enhancing stem-like tumor-reactive CD8

Tichet, Mélanie / Wullschleger, Stephan / Chryplewicz, Agnieszka / Fournier, Nadine / Marcone, Rachel / Kauzlaric, Annamaria / Homicsko, Krisztian / Deak, Laura Codarri / Umaña, Pablo / Klein, Christian / Hanahan, Douglas

Immunity

2023 Volume 56, Issue 1, Page(s) 162–179.e6

Abstract: Immunotherapies have shown remarkable, albeit tumor-selective, therapeutic benefits in the clinic. Most patients respond transiently at best, highlighting the importance of understanding mechanisms underlying resistance. Herein, we evaluated the effects ... ...

Abstract	Immunotherapies have shown remarkable, albeit tumor-selective, therapeutic benefits in the clinic. Most patients respond transiently at best, highlighting the importance of understanding mechanisms underlying resistance. Herein, we evaluated the effects of the engineered immunocytokine PD1-IL2v in a mouse model of de novo pancreatic neuroendocrine cancer that is resistant to checkpoint and other immunotherapies. PD1-IL2v utilizes anti-PD-1 as a targeting moiety fused to an immuno-stimulatory IL-2 cytokine variant (IL2v) to precisely deliver IL2v to PD-1
MeSH term(s)	Animals ; Mice ; B7-H1 Antigen/immunology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Disease Models, Animal ; Immunotherapy/methods ; Macrophages/immunology ; Macrophages/metabolism ; Neoplasms/therapy ; Tumor Microenvironment ; Antibodies, Bispecific/immunology ; Interleukin-2 ; Programmed Cell Death 1 Receptor/immunology
Chemical Substances	B7-H1 Antigen ; Antibodies, Bispecific ; Interleukin-2 ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2023-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2022.12.006
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Article ; Online: ALK7 Signaling Manifests a Homeostatic Tissue Barrier That Is Abrogated during Tumorigenesis and Metastasis.

Michael, Iacovos P / Saghafinia, Sadegh / Tichet, Mélanie / Zangger, Nadine / Marinoni, Ilaria / Perren, Aurel / Hanahan, Douglas

Developmental cell

2019 Volume 49, Issue 3, Page(s) 409–424.e6

Abstract: Herein, we report that the TGFß superfamily receptor ALK7 is a suppressor of tumorigenesis and metastasis, as revealed by functional studies in mouse models of pancreatic neuroendocrine and luminal breast cancer, complemented by experimental metastasis ... ...

Abstract	Herein, we report that the TGFß superfamily receptor ALK7 is a suppressor of tumorigenesis and metastasis, as revealed by functional studies in mouse models of pancreatic neuroendocrine and luminal breast cancer, complemented by experimental metastasis assays. Activation in neoplastic cells of the ALK7 signaling pathway by its principal ligand activin B induces apoptosis. During tumorigenesis, cancer cells use two different approaches to evade this barrier, either downregulating activin B and/or downregulating ALK7. Suppressing ALK7 expression additionally contributes to the capability for metastatic seeding. ALK7 is associated with shorter relapse-free survival of various human cancers and distant-metastasis-free survival of breast cancer patients. This study introduces mechanistic insights into primary and metastatic tumor development, in the form of a protective barrier that triggers apoptosis in cells that are not "authorized" to proliferate within a particular tissue, by virtue of those cells expressing ALK7 in a tissue microenvironment bathed in its ligand.
MeSH term(s)	Activin Receptors, Type I/metabolism ; Activins/metabolism ; Animals ; Apoptosis/physiology ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Carcinogenesis ; Cell Line, Tumor ; Cell Transformation, Neoplastic/metabolism ; Female ; Heterografts ; Homeostasis ; Humans ; Male ; Mice ; Mice, Inbred A ; Mice, Inbred C57BL ; Mice, SCID ; Neoplasm Metastasis ; Neoplasms/metabolism ; Neoplasms/pathology ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Signal Transduction ; Smad2 Protein/metabolism ; Transforming Growth Factor beta/metabolism ; Tumor Microenvironment
Chemical Substances	Smad2 Protein ; Transforming Growth Factor beta ; activin B ; Activins (104625-48-1) ; ACVR1C protein, human (EC 2.7.11.30) ; Activin Receptors, Type I (EC 2.7.11.30)
Language	English
Publishing date	2019-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2019.04.015
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Zs.A 5742: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Nanoparticle Conjugation of Human Papillomavirus 16 E7-long Peptides Enhances Therapeutic Vaccine Efficacy against Solid Tumors in Mice.

Galliverti, Gabriele / Tichet, Mélanie / Domingos-Pereira, Sonia / Hauert, Sylvie / Nardelli-Haefliger, Denise / Swartz, Melody A / Hanahan, Douglas / Wullschleger, Stephan

Cancer immunology research

2018 Volume 6, Issue 11, Page(s) 1301–1313

Abstract: Treatment of patients bearing human papillomavirus (HPV)-related cancers with synthetic long-peptide (SLP) therapeutic vaccines has shown promising results in clinical trials against premalignant lesions, whereas responses against later stage carcinomas ... ...

Abstract	Treatment of patients bearing human papillomavirus (HPV)-related cancers with synthetic long-peptide (SLP) therapeutic vaccines has shown promising results in clinical trials against premalignant lesions, whereas responses against later stage carcinomas have remained elusive. We show that conjugation of a well-documented HPV-E7 SLP to ultra-small polymeric nanoparticles (NP) enhances the antitumor efficacy of therapeutic vaccination in different mouse models of HPV
MeSH term(s)	Animals ; Antibodies/pharmacology ; CD8-Positive T-Lymphocytes/immunology ; Cancer Vaccines/chemistry ; Cancer Vaccines/immunology ; Cancer Vaccines/pharmacology ; Female ; Lung Neoplasms/secondary ; Mice, Inbred C57BL ; Mice, Transgenic ; Nanoparticles/chemistry ; Neoplasm Recurrence, Local ; Neoplasms, Experimental/immunology ; Neoplasms, Experimental/mortality ; Neoplasms, Experimental/therapy ; Papillomavirus E7 Proteins/chemistry ; Papillomavirus E7 Proteins/immunology ; Papillomavirus E7 Proteins/pharmacology ; T-Lymphocytes, Regulatory/immunology ; Treatment Outcome ; Tumor Necrosis Factor Receptor Superfamily, Member 9/immunology ; Vaginal Neoplasms/immunology ; Vaginal Neoplasms/pathology ; Vaginal Neoplasms/prevention & control
Chemical Substances	Antibodies ; Cancer Vaccines ; Papillomavirus E7 Proteins ; Tumor Necrosis Factor Receptor Superfamily, Member 9 ; oncogene protein E7, Human papillomavirus type 16
Language	English
Publishing date	2018-08-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-18-0166
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Article ; Online: Aberrant hyperexpression of the RNA binding protein FMRP in tumors mediates immune evasion.

Science (New York, N.Y.)

2022 Volume 378, Issue 6621, Page(s) eabl7207

Abstract: Many human cancers manifest the capability to circumvent attack by the adaptive immune system. In this work, we identified a component of immune evasion that involves frequent up-regulation of fragile X mental retardation protein (FMRP) in solid tumors. ... ...

Abstract	Many human cancers manifest the capability to circumvent attack by the adaptive immune system. In this work, we identified a component of immune evasion that involves frequent up-regulation of fragile X mental retardation protein (FMRP) in solid tumors. FMRP represses immune attack, as revealed by cancer cells engineered to lack its expression. FMRP-deficient tumors were infiltrated by activated T cells that impaired tumor growth and enhanced survival in mice. Mechanistically, FMRP's immunosuppression was multifactorial, involving repression of the chemoattractant C-C motif chemokine ligand 7 (CCL7) concomitant with up-regulation of three immunomodulators-interleukin-33 (IL-33), tumor-secreted protein S (PROS1), and extracellular vesicles. Gene signatures associate FMRP's cancer network with poor prognosis and response to therapy in cancer patients. Collectively, FMRP is implicated as a regulator that orchestrates a multifaceted barrier to antitumor immune responses.
MeSH term(s)	Animals ; Humans ; Mice ; Fragile X Mental Retardation Protein/genetics ; Fragile X Mental Retardation Protein/metabolism ; Immune Evasion ; Neoplasms/immunology ; Immune Tolerance ; Chemokine CCL7/metabolism ; Interleukin-33 ; Protein S/metabolism
Chemical Substances	Fragile X Mental Retardation Protein (139135-51-6) ; FMR1 protein, human ; Chemokine CCL7 ; Interleukin-33 ; PROS1 protein, human ; Protein S
Language	English
Publishing date	2022-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.abl7207
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Zs.A 27: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Risk for nevus transformation and melanoma proliferation and invasion during natalizumab treatment: four years of dermoscopic follow-up with immunohistological studies and proliferation and invasion assays.

Pharaon, Momen / Tichet, Mélanie / Lebrun-Frénay, Christine / Tartare-Deckert, Sophie / Passeron, Thierry

JAMA dermatology

2014 Volume 150, Issue 8, Page(s) 901–903

MeSH term(s)	Antibodies, Monoclonal, Humanized/pharmacology ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cell Transformation, Neoplastic ; Dermoscopy ; Follow-Up Studies ; Humans ; Immunohistochemistry ; Immunologic Factors/pharmacology ; Integrin beta3/analysis ; Melanoma/chemistry ; Melanoma/pathology ; Multiple Sclerosis/drug therapy ; Natalizumab ; Nevus/chemistry ; Nevus/pathology ; Osteonectin/analysis ; Skin Neoplasms/chemistry ; Skin Neoplasms/pathology
Chemical Substances	Antibodies, Monoclonal, Humanized ; Immunologic Factors ; Integrin beta3 ; Natalizumab ; Osteonectin ; SPARC protein, human
Language	English
Publishing date	2014-08
Publishing country	United States
Document type	Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	2701761-8
ISSN	2168-6084 ; 2168-6068
ISSN (online)	2168-6084
ISSN	2168-6068
DOI	10.1001/jamadermatol.2013.9411
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Article ; Online: Myeloid Cells Orchestrate Systemic Immunosuppression, Impairing the Efficacy of Immunotherapy against HPV

Galliverti, Gabriele / Wullschleger, Stephan / Tichet, Mélanie / Murugan, Dhaarini / Zangger, Nadine / Horton, Wesley / Korman, Alan J / Coussens, Lisa M / Swartz, Melody A / Hanahan, Douglas

Cancer immunology research

2019 Volume 8, Issue 1, Page(s) 131–145

Abstract: Cancers induced by human papillomaviruses (HPV) should be responsive to immunotherapy by virtue of expressing the immunogenic oncoproteins E6/E7. However, advanced forms of cervical cancer, driven by HPV, are poorly responsive to immune response- ... ...

Abstract	Cancers induced by human papillomaviruses (HPV) should be responsive to immunotherapy by virtue of expressing the immunogenic oncoproteins E6/E7. However, advanced forms of cervical cancer, driven by HPV, are poorly responsive to immune response-enhancing treatments involving therapeutic vaccination against these viral neoantigens. Leveraging a transgenic mouse model of HPV-derived cancers, K14HPV16/H2b, we demonstrated that a potent nanoparticle-based E7 vaccine, but not a conventional "liquid" vaccine, induced E7 tumor antigen-specific CD8
MeSH term(s)	Animals ; Antineoplastic Agents, Immunological/pharmacology ; CD8-Positive T-Lymphocytes/immunology ; CTLA-4 Antigen/antagonists & inhibitors ; Disease Models, Animal ; Drug Synergism ; Female ; Humans ; Immunosuppression Therapy ; Immunotherapy/methods ; Mice ; Myeloid Cells/drug effects ; Myeloid Cells/immunology ; Nanoparticles/administration & dosage ; Papillomaviridae/immunology ; Papillomavirus E7 Proteins/immunology ; Papillomavirus E7 Proteins/metabolism ; Papillomavirus Infections/drug therapy ; Papillomavirus Infections/immunology ; Papillomavirus Infections/virology ; Papillomavirus Vaccines/administration & dosage ; Papillomavirus Vaccines/immunology ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Tumor Microenvironment ; Uterine Cervical Neoplasms/drug therapy ; Uterine Cervical Neoplasms/immunology ; Uterine Cervical Neoplasms/pathology ; Uterine Cervical Neoplasms/virology
Chemical Substances	Antineoplastic Agents, Immunological ; CTLA-4 Antigen ; Ctla4 protein, mouse ; Papillomavirus E7 Proteins ; Papillomavirus Vaccines ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2019-11-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-19-0315
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Article ; Online: Targeting the Proteasome-Associated Deubiquitinating Enzyme USP14 Impairs Melanoma Cell Survival and Overcomes Resistance to MAPK-Targeting Therapies.

Didier, Robin / Mallavialle, Aude / Ben Jouira, Rania / Domdom, Marie Angela / Tichet, Mélanie / Auberger, Patrick / Luciano, Frédéric / Ohanna, Mickael / Tartare-Deckert, Sophie / Deckert, Marcel

Molecular cancer therapeutics

2018 Volume 17, Issue 7, Page(s) 1416–1429

Abstract: Advanced cutaneous melanoma is one of the most challenging cancers to treat because of its high plasticity, metastatic potential, and resistance to treatment. New targeted therapies and immunotherapies have shown remarkable clinical efficacy. However, ... ...

Abstract	Advanced cutaneous melanoma is one of the most challenging cancers to treat because of its high plasticity, metastatic potential, and resistance to treatment. New targeted therapies and immunotherapies have shown remarkable clinical efficacy. However, such treatments are limited to a subset of patients and relapses often occur, warranting validation of novel targeted therapies. Posttranslational modification of proteins by ubiquitin coordinates essential cellular functions, including ubiquitin-proteasome system (UPS) function and protein homeostasis. Deubiquitinating enzymes (DUB) have been associated to multiple diseases, including cancer. However, their exact involvement in melanoma development and therapeutic resistance remains poorly understood. Using a DUB trap assay to label cellular active DUBs, we have observed an increased activity of the proteasome-associated DUB, USP14 (Ubiquitin-specific peptidase 14) in melanoma cells compared with melanocytes. Our survey of public gene expression databases indicates that high expression of
MeSH term(s)	Animals ; Apoptosis/drug effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Deubiquitinating Enzymes/antagonists & inhibitors ; Deubiquitinating Enzymes/genetics ; Drug Resistance, Neoplasm/genetics ; GTP Phosphohydrolases/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; MAP Kinase Kinase 1/genetics ; Melanocytes/drug effects ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/pathology ; Membrane Proteins/genetics ; Mice ; Molecular Targeted Therapy ; Proteasome Inhibitors/pharmacology ; Proto-Oncogene Proteins B-raf/genetics ; Reactive Oxygen Species/metabolism ; Tumor Suppressor Protein p53/genetics ; Ubiquitin Thiolesterase/antagonists & inhibitors ; Ubiquitin Thiolesterase/genetics ; Xenograft Model Antitumor Assays
Chemical Substances	Membrane Proteins ; Proteasome Inhibitors ; Reactive Oxygen Species ; TP53 protein, human ; Tumor Suppressor Protein p53 ; USP14 protein, human ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; Deubiquitinating Enzymes (EC 3.4.19.12) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; GTP Phosphohydrolases (EC 3.6.1.-) ; NRAS protein, human (EC 3.6.1.-)
Language	English
Publishing date	2018-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-17-0919
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Article ; Online: PD-1-cis IL-2R agonism yields better effectors from stem-like CD8

Codarri Deak, Laura / Nicolini, Valeria / Hashimoto, Masao / Karagianni, Maria / Schwalie, Petra C / Lauener, Laura / Varypataki, Eleni Maria / Richard, Marine / Bommer, Esther / Sam, Johannes / Joller, Stefanie / Perro, Mario / Cremasco, Floriana / Kunz, Leo / Yanguez, Emilio / Hüsser, Tamara / Schlenker, Ramona / Mariani, Marisa / Tosevski, Vinko /

Herter, Sylvia / Bacac, Marina / Waldhauer, Inja / Colombetti, Sara / Gueripel, Xavier / Wullschleger, Stephan / Tichet, Melanie / Hanahan, Douglas / Kissick, Haydn T / Leclair, Stephane / Freimoser-Grundschober, Anne / Seeber, Stefan / Teichgräber, Volker / Ahmed, Rafi / Klein, Christian / Umaña, Pablo

Nature

2022 Volume 610, Issue 7930, Page(s) 161–172

Abstract: Expansion and differentiation of antigen-experienced PD- ... ...

Abstract	Expansion and differentiation of antigen-experienced PD-1
MeSH term(s)	Antibodies, Blocking/immunology ; Antibodies, Blocking/pharmacology ; Antibodies, Blocking/therapeutic use ; B7-H1 Antigen/antagonists & inhibitors ; B7-H1 Antigen/immunology ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; Infections/drug therapy ; Infections/immunology ; Interleukin-2/immunology ; Interleukin-2/pharmacology ; Interleukin-2/therapeutic use ; Interleukin-2 Receptor alpha Subunit/agonists ; Neoplasms/drug therapy ; Neoplasms/immunology ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Receptors, Interleukin-2/agonists
Chemical Substances	Antibodies, Blocking ; B7-H1 Antigen ; Interleukin-2 ; Interleukin-2 Receptor alpha Subunit ; Programmed Cell Death 1 Receptor ; Receptors, Interleukin-2
Language	English
Publishing date	2022-09-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-022-05192-0
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Zs.A 26: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Tumour-derived SPARC drives vascular permeability and extravasation through endothelial VCAM1 signalling to promote metastasis.

Tichet, Mélanie / Prod'Homme, Virginie / Fenouille, Nina / Ambrosetti, Damien / Mallavialle, Aude / Cerezo, Michael / Ohanna, Mickaël / Audebert, Stéphane / Rocchi, Stéphane / Giacchero, Damien / Boukari, Fériel / Allegra, Maryline / Chambard, Jean-Claude / Lacour, Jean-Philippe / Michiels, Jean-François / Borg, Jean-Paul / Deckert, Marcel / Tartare-Deckert, Sophie

Nature communications

2015 Volume 6, Page(s) 6993

Abstract: Disruption of the endothelial barrier by tumour-derived secreted factors is a critical step in cancer cell extravasation and metastasis. Here, by comparative proteomic analysis of melanoma secretomes, we identify the matricellular protein SPARC as a ... ...

Abstract	Disruption of the endothelial barrier by tumour-derived secreted factors is a critical step in cancer cell extravasation and metastasis. Here, by comparative proteomic analysis of melanoma secretomes, we identify the matricellular protein SPARC as a novel tumour-derived vascular permeability factor. SPARC deficiency abrogates tumour-initiated permeability of lung capillaries and prevents extravasation, whereas SPARC overexpression enhances vascular leakiness, extravasation and lung metastasis. SPARC-induced paracellular permeability is dependent on the endothelial VCAM1 receptor and p38 MAPK signalling. Blocking VCAM1 impedes melanoma-induced endothelial permeability and extravasation. The clinical relevance of our findings is highlighted by high levels of SPARC detected in tumour from human pulmonary melanoma lesions. Our study establishes tumour-produced SPARC and VCAM1 as regulators of cancer extravasation, revealing a novel targetable interaction for prevention of metastasis.
MeSH term(s)	Animals ; Capillary Permeability ; Case-Control Studies ; Cell Line, Tumor ; Endothelium, Vascular/metabolism ; Female ; Human Umbilical Vein Endothelial Cells ; Humans ; Lung Neoplasms/secondary ; MAP Kinase Signaling System ; Melanoma/metabolism ; Melanoma/pathology ; Melanoma/secretion ; Mice, Nude ; Neoplasm Metastasis ; Osteonectin/metabolism ; Paracrine Communication ; Vascular Cell Adhesion Molecule-1/metabolism
Chemical Substances	Osteonectin ; SPARC protein, human ; Vascular Cell Adhesion Molecule-1
Language	English
Publishing date	2015-04-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms7993
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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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Order via subito

Inter-library loan at ZB MED