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Article ; Online: HaCaT cells as a model system to study primary cilia in keratinocytes.

Blanchard, Gabriela / Pich, Christine / Hohl, Daniel

2022 Volume 31, Issue 8, Page(s) 1276–1280

Abstract: Primary cilium (PC) is a microtubule-based organelle found on the apical surface of most mammalian cell types, playing a role in development and tissue homeostasis. Ciliopathies are a rapidly growing group of human diseases characterized by disordered ... ...

Abstract	Primary cilium (PC) is a microtubule-based organelle found on the apical surface of most mammalian cell types, playing a role in development and tissue homeostasis. Ciliopathies are a rapidly growing group of human diseases characterized by disordered cilium. PC plays an important role in pathogenesis of basal cell cancer, the most common human malignancy. A significant increase in ciliation has been observed in the epidermis of atopic dermatitis and psoriasis patients. Spontaneously immortalized human keratinocytes, HaCaT are a model to study the epidermal homeostasis and pathophysiology. In contrast to what has been previously described, here, we show that HaCaT can be efficiently ciliated. In HaCaT cells, differentiation significantly increased the number of ciliated cells and we were able to analyse in detail the ciliary length progression with duration of differentiation. As the number of recognized ciliopathies continues to increase, the importance of ciliary models also rises. Even though keratinocytes do not become as highly and rapidly ciliated as cell lines frequently used in ciliary studies, they are a better model for the study of skin ciliopathies. Detailed progression of ciliation in HaCaT could serve as the basis for ciliary studies in this cell line.
MeSH term(s)	Animals ; Cilia/metabolism ; Ciliopathies/metabolism ; Epidermis ; HaCaT Cells ; Humans ; Keratinocytes/metabolism ; Mammals
Language	English
Publishing date	2022-06-23
Publishing country	Denmark
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1130936-2
ISSN	1600-0625 ; 0906-6705
ISSN (online)	1600-0625
ISSN	0906-6705
DOI	10.1111/exd.14626
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Article ; Online: The Janus face of rosiglitazone.

Pich, Christine / Michalik, Liliane

Oncotarget

2018 Volume 9, Issue 102, Page(s) 37614–37615

Language	English
Publishing date	2018-12-28
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.26532
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Article ; Online: Itraconazole resistance of Trichophyton rubrum mediated by the ABC transporter TruMDR2.

Yamada, Tsuyoshi / Yaguchi, Takashi / Tamura, Takashi / Pich, Christine / Salamin, Karine / Feuermann, Marc / Monod, Michel

Mycoses

2021 Volume 64, Issue 8, Page(s) 936–946

Abstract: Background: Dermatophytes showing reduced sensitivity to antifungal agents have emerged in several countries. One terbinafine resistant strain of Trichophyton rubrum, TIMM20092, also showed reduced sensitivity to itraconazole (ITC) and voriconazole (VRC) ...

Abstract	Background: Dermatophytes showing reduced sensitivity to antifungal agents have emerged in several countries. One terbinafine resistant strain of Trichophyton rubrum, TIMM20092, also showed reduced sensitivity to itraconazole (ITC) and voriconazole (VRC). The expression of two genes (TruMDR2 and TruMDR3) encoding multidrug transporters of the ABC family was found to be highly up-regulated in this strain. Deletion of TruMDR3 in TIMM20092 abolished its resistance to VRC but only slightly reduced its resistance to ITC. Objectives: We examined the potential of T rubrum to develop resistance to ITC by analysing the mechanism of ITC resistance in TIMM20092. Methods: The deletion of TruMDR2 by gene replacement was performed in TIMM20092 and one TruMDR3-lacking mutant (∆TruMDR3) previously generated from TIMM20092. TruMDR2 single and TruMDR2/TruMDR3 double mutants (∆TruMDR2 and ∆TruMDR2/3) were successfully obtained, respectively. Results: The suppression of TruMDR2 was shown to abolish resistance to ITC in TIMM20092 and the TruMDR3-lacking mutant, strongly suggesting that TruMDR2 is a major contributor to ITC resistance in TIMM20092. Conclusions: Our study highlights the possible role of the ABC transporter TruMDR2 in ITC resistance of T. rubrum.
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily B/genetics ; ATP Binding Cassette Transporter, Subfamily B/metabolism ; Antifungal Agents/pharmacology ; Arthrodermataceae/drug effects ; Arthrodermataceae/genetics ; Drug Resistance, Fungal/genetics ; Humans ; Itraconazole/pharmacology ; Microbial Sensitivity Tests ; ATP-Binding Cassette Sub-Family B Member 4
Chemical Substances	ATP Binding Cassette Transporter, Subfamily B ; Antifungal Agents ; Itraconazole (304NUG5GF4)
Language	English
Publishing date	2021-04-25
Publishing country	Germany
Document type	Journal Article
ZDB-ID	392487-7
ISSN	1439-0507 ; 0933-7407
ISSN (online)	1439-0507
ISSN	0933-7407
DOI	10.1111/myc.13286
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Article ; Online: Regulatory properties of statins and rho gtpases prenylation inhibitiors to stimulate melanoma immunogenicity and promote anti-melanoma immune response.

Sarrabayrouse, Guillaume / Pich, Christine / Teiti, Iotefa / Tilkin-Mariame, Anne Françoise

International journal of cancer

2017 Volume 140, Issue 4, Page(s) 747–755

Abstract: Melanoma is a highly lethal cutaneous tumor, killing affected patients through development of multiple poorly immunogenic metastases. Suboptimal activation of immune system by melanoma cells is often due to molecular modifications occurring during tumor ... ...

Abstract	Melanoma is a highly lethal cutaneous tumor, killing affected patients through development of multiple poorly immunogenic metastases. Suboptimal activation of immune system by melanoma cells is often due to molecular modifications occurring during tumor progression that prevent efficient recognition of melanoma cells by immune effectors. Statins are HMG-CoA reductase inhibitors, which block the mevalonate synthesis pathway, used by millions of people as hypocholesterolemic agents in cardiovascular and cerebrovascular diseases. They are also known to inhibit Rho GTPase activation and Rho dependent signaling pathways. Rho GTPases are regarded as molecular switches that regulate a wide spectrum of cellular functions and their dysfunction has been characterized in various oncogenic process notably in melanoma progression. Moreover, these molecules can modulate the immune response. Since 10 years we have demonstrated that Statins and other Rho GTPases inhibitors are critical regulators of molecules involved in adaptive and innate anti-melanoma immune response. In this review we summarize our major observations demonstrating that these pharmacological agents stimulate melanoma immunogenicity and suggest a potential use of these molecules to promote anti-melanoma immune response.
MeSH term(s)	Adaptive Immunity/drug effects ; Adjuvants, Immunologic/pharmacology ; Adjuvants, Immunologic/therapeutic use ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Disease Progression ; Enzyme Activation/drug effects ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Immunity, Innate/drug effects ; Melanoma/drug therapy ; Melanoma/immunology ; Melanoma, Experimental/drug therapy ; Melanoma, Experimental/immunology ; Mevalonic Acid/metabolism ; Mice ; Molecular Targeted Therapy ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/physiology ; Protein Prenylation/drug effects ; Signal Transduction/drug effects ; rho GTP-Binding Proteins/antagonists & inhibitors ; rho GTP-Binding Proteins/physiology
Chemical Substances	Adjuvants, Immunologic ; Antineoplastic Agents ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Neoplasm Proteins ; rho GTP-Binding Proteins (EC 3.6.5.2) ; Mevalonic Acid (S5UOB36OCZ)
Language	English
Publishing date	2017-02-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.30422
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Zs.A 478: 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: Low expression of the PPARγ-regulated gene thioredoxin-interacting protein accompanies human melanoma progression and promotes experimental lung metastases.

Meylan, Patrick / Pich, Christine / Winkler, Carine / Ginster, Stefanie / Mury, Lionel / Sgandurra, Marie / Dreos, René / Frederick, Dennie Tompers / Hammond, Marc / Boland, Genevieve Marie / Michalik, Liliane

Scientific reports

2021 Volume 11, Issue 1, Page(s) 7847

Abstract: The thioredoxin system plays key roles in regulating cancer cell malignancy. Here we identify the Thioredoxin-interacting protein (TXNIP) as a gene, which expression is regulated by PPARγ in melanoma cells. We show that high TXNIP expression levels ... ...

Abstract	The thioredoxin system plays key roles in regulating cancer cell malignancy. Here we identify the Thioredoxin-interacting protein (TXNIP) as a gene, which expression is regulated by PPARγ in melanoma cells. We show that high TXNIP expression levels associate with benign melanocytic lesions, with tumor regression in patients on MAP kinase targeted therapy, with decreased proliferation in patients' melanoma biopsies, and with cell cycle arrest in human melanoma cell lines. In contrast, reduced TXNIP expression associates with advanced melanoma and with disease progression in patients. TXNIP depletion in human melanoma cells altered the expression of integrin beta-3 and the localization of the integrin alpha-v/beta-3 dimer at their surface. Moreover, TXNIP depletion affected human melanoma cell motility and improved their capacity to colonize mouse lungs in an in vivo assay. This study establishes TXNIP as a PPARγ-regulated gene in melanoma cells, thereby suggesting a link between these two proteins both involved in the regulation of cancer and of energy metabolism. It also reveals that the decrease in TXNIP expression, which is observed in advanced patient tumors, likely favors lung metastatic seeding of malignant cells.
MeSH term(s)	Animals ; Carrier Proteins/metabolism ; Cell Line, Tumor ; Female ; Humans ; Lung Neoplasms/metabolism ; Lung Neoplasms/secondary ; Melanoma/metabolism ; Melanoma/pathology ; Mice ; PPAR gamma/metabolism
Chemical Substances	Carrier Proteins ; PPAR gamma ; PPARG protein, human ; TXNIP protein, human
Language	English
Publishing date	2021-04-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-86329-5
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Article ; Online: ARP-T1-associated Bazex-Dupré-Christol syndrome is an inherited basal cell cancer with ciliary defects characteristic of ciliopathies.

Park, Hyun-Sook / Papanastasi, Eirini / Blanchard, Gabriela / Chiticariu, Elena / Bachmann, Daniel / Plomann, Markus / Morice-Picard, Fanny / Vabres, Pierre / Smahi, Asma / Huber, Marcel / Pich, Christine / Hohl, Daniel

Communications biology

2021 Volume 4, Issue 1, Page(s) 544

Abstract: Actin-Related Protein-Testis1 (ARP-T1)/ACTRT1 gene mutations cause the Bazex-Dupré-Christol Syndrome (BDCS) characterized by follicular atrophoderma, hypotrichosis, and basal cell cancer. Here, we report an ARP-T1 interactome (PXD016557) that includes ... ...

Abstract	Actin-Related Protein-Testis1 (ARP-T1)/ACTRT1 gene mutations cause the Bazex-Dupré-Christol Syndrome (BDCS) characterized by follicular atrophoderma, hypotrichosis, and basal cell cancer. Here, we report an ARP-T1 interactome (PXD016557) that includes proteins involved in ciliogenesis, endosomal recycling, and septin ring formation. In agreement, ARP-T1 localizes to the midbody during cytokinesis and the basal body of primary cilia in interphase. Tissue samples from ARP-T1-associated BDCS patients have reduced ciliary length. The severity of the shortened cilia significantly correlates with the ARP-T1 levels, which was further validated by ACTRT1 knockdown in culture cells. Thus, we propose that ARP-T1 participates in the regulation of cilia length and that ARP-T1-associated BDCS is a case of skin cancer with ciliopathy characteristics.
MeSH term(s)	Carcinoma, Basal Cell/genetics ; Carcinoma, Basal Cell/metabolism ; Carcinoma, Basal Cell/pathology ; Cilia/metabolism ; Cilia/pathology ; Ciliopathies/genetics ; Ciliopathies/metabolism ; Ciliopathies/pathology ; Humans ; Hypotrichosis/genetics ; Hypotrichosis/metabolism ; Hypotrichosis/pathology ; Keratinocytes/metabolism ; Keratinocytes/pathology ; Microfilament Proteins/genetics ; Microfilament Proteins/metabolism ; Mutation ; Neoplasms, Basal Cell/genetics ; Neoplasms, Basal Cell/metabolism ; Neoplasms, Basal Cell/pathology ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology
Chemical Substances	ACTRT1 protein, human ; Microfilament Proteins
Language	English
Publishing date	2021-05-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-021-02054-9
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Article ; Online: Melanoma Expressed-CD70 Is Regulated by RhoA and MAPK Pathways without Affecting Vemurafenib Treatment Activity.

Pich, Christine / Teiti, Iotefa / Sarrabayrouse, Guillaume / Gallardo, Franck / Gence, Rémi / Tilkin-Mariamé, Anne-Françoise

PloS one

2016 Volume 11, Issue 2, Page(s) e0148095

Abstract: CD70 is a costimulatory molecule member of the Tumor Necrosis Factor family that is expressed on activated immune cells. Its ectopic expression has been described in several types of cancer cells including lymphomas, renal cell carcinomas and ... ...

Abstract	CD70 is a costimulatory molecule member of the Tumor Necrosis Factor family that is expressed on activated immune cells. Its ectopic expression has been described in several types of cancer cells including lymphomas, renal cell carcinomas and glioblastomas. We have recently described its expression in a part of tumor cells from the vast majority of melanoma biopsies and human melanoma cell lines, and found that CD70 expression decreased over time as the disease progressed. Here, we show that RhoA, BRAF and Mitogen Activating Protein Kinase pathways are involved in the positive transcriptional regulation of CD70 expression in melanomas. Interestingly, the clinical inhibitor of the common BRAF V600E/D variants, Vemurafenib (PLX-4032), which is currently used to treat melanoma patients with BRAF V600E/D-mutated metastatic melanomas, decreased CD70 expression in human CD70+ melanoma cell lines. This decrease was seen in melanoma cells both with and without the BRAFV600E/D mutation, although was less efficient in those lacking the mutation. But interestingly, by silencing CD70 in CD70+ melanoma cell lines we show that PLX-4032-induced melanoma cell killing and its inhibitory effect on MAPK pathway activation are unaffected by CD70 expression. Consequently, our work demonstrates that CD70 ectopic expression in melanomas is not a valuable biomarker to predict tumor cells sensitivity to BRAF V600 inhibitors.
MeSH term(s)	CD27 Ligand/metabolism ; Cell Line, Tumor ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Cell Proliferation/drug effects ; Gene Silencing/drug effects ; Humans ; Indoles/pharmacology ; Indoles/therapeutic use ; MAP Kinase Signaling System/drug effects ; Melanoma/drug therapy ; Melanoma/enzymology ; Melanoma/genetics ; Melanoma/pathology ; Proto-Oncogene Proteins B-raf/metabolism ; Skin Neoplasms ; Sulfonamides/pharmacology ; Sulfonamides/therapeutic use ; Transcription, Genetic/drug effects ; Vemurafenib ; rhoA GTP-Binding Protein/metabolism ; Melanoma, Cutaneous Malignant
Chemical Substances	CD27 Ligand ; Indoles ; Sulfonamides ; Vemurafenib (207SMY3FQT) ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2016-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0148095
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Article ; Online: Melanoma-expressed CD70 is involved in invasion and metastasis.

Pich, Christine / Sarrabayrouse, Guillaume / Teiti, Iotefa / Mariamé, Bernard / Rochaix, Philippe / Lamant, Laurence / Favre, Gilles / Maisongrosse, Véronique / Tilkin-Mariamé, Anne-Françoise

British journal of cancer

2016 Volume 114, Issue 1, Page(s) 63–70

Abstract: Background: CD70 is a costimulatory molecule of the tumour necrosis factor family expressed in activated immune cells and some solid tumours. In lymphocytes CD70 triggers T cell-mediated cytotoxicity and mitogen-activated protein kinase phosphorylation.! ...

Abstract	Background: CD70 is a costimulatory molecule of the tumour necrosis factor family expressed in activated immune cells and some solid tumours. In lymphocytes CD70 triggers T cell-mediated cytotoxicity and mitogen-activated protein kinase phosphorylation. Methods: We evaluated the expression of CD70 in biopsies and melanoma cell lines. Using melanoma cell lines positive or not for CD70, we analysed CD70 function on melanoma progression. Results: We report CD70 expression in human melanoma cell lines and tumour cells from melanoma biopsies. This expression was observed in 95% of primary melanomas but only 37% of metastases. Both monomeric and trimeric forms of CD70 were detected in tumour cell membrane fractions, whereas cytoplasmic fractions contained almost exclusively monomeric CD70. In vitro and in vivo experiments demonstrated that CD70 expression inhibited melanoma cell migration, invasion and pulmonary metastasis implantation independently of the tumour immune microenvironment. Increasing the levels of the trimeric form of CD70 through monoclonal antibody binding led to an increase in CD70+ melanoma cell invasiveness through MAPK pathway activation, RhoE overexpression, ROCK1 and MYPT1 phosphorylation decrease, and stress fibres and focal adhesions disappearance. Conclusions: Our results describe a new non-immunological function of melanoma-expressed CD70, which involves melanoma invasiveness through MAPK pathway, RhoE and cytoskeletal modulation.
MeSH term(s)	Animals ; CD27 Ligand/analysis ; CD27 Ligand/physiology ; Cell Line, Tumor ; Cell Movement ; Cytoskeleton/physiology ; Female ; Humans ; MAP Kinase Signaling System/physiology ; Melanoma/pathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Invasiveness ; Neoplasm Metastasis ; rho GTP-Binding Proteins/physiology ; rho-Associated Kinases/physiology
Chemical Substances	CD27 Ligand ; CD70 protein, human ; ROCK1 protein, human (EC 2.7.11.1) ; rho-Associated Kinases (EC 2.7.11.1) ; RND3 protein, human (EC 3.6.5.2) ; rho GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2016-01-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/bjc.2015.412
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Article ; Online: Induction of Paracrine Signaling in Metastatic Melanoma Cells by PPARγ Agonist Rosiglitazone Activates Stromal Cells and Enhances Tumor Growth.

Pich, Christine / Meylan, Patrick / Mastelic-Gavillet, Beatris / Nguyen, Thanh Nhan / Loyon, Romain / Trang, Bao Khanh / Moser, Hélène / Moret, Catherine / Goepfert, Christine / Hafner, Jürg / Levesque, Mitchell P / Romero, Pedro / Jandus, Camilla / Michalik, Liliane

Cancer research

2018 Volume 78, Issue 22, Page(s) 6447–6461

Abstract: In addition to improving insulin sensitivity in type 2 diabetes, the thiazolidinedione family of compounds and the pharmacologic activation of their best-characterized target PPARγ have been proposed as a therapeutic option for cancer treatment. In this ... ...

Abstract	In addition to improving insulin sensitivity in type 2 diabetes, the thiazolidinedione family of compounds and the pharmacologic activation of their best-characterized target PPARγ have been proposed as a therapeutic option for cancer treatment. In this study, we reveal a new mode of action for the thiazolidinedione rosiglitazone that can contribute to tumorigenesis. Rosiglitazone activated a tumorigenic paracrine communication program in a subset of human melanoma cells that involves the secretion of cytokines, chemokines, and angiogenic factors. This complex blend of paracrine signals activated nonmalignant fibroblasts, endothelial cells, and macrophages in a tumor-friendly way. In agreement with these data, rosiglitazone promoted human melanoma development in xenografts, and tumors exposed to rosiglitazone exhibited enhanced angiogenesis and inflammation. Together, these findings establish an important tumorigenic action of rosiglitazone in a subset of melanoma cells. Although studies conducted on cohorts of diabetic patients report overall benefits of thiazolidinediones in cancer prevention, our data suggest that exposure of established tumors to rosiglitazone may be deleterious.
MeSH term(s)	Angiogenesis Inducing Agents/metabolism ; Animals ; Carcinogenesis ; Cell Line, Tumor ; Fibroblasts/metabolism ; Human Umbilical Vein Endothelial Cells/drug effects ; Humans ; Inflammation ; Leukocytes, Mononuclear/cytology ; Macrophages/drug effects ; Melanoma/metabolism ; Melanoma/pathology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Monocytes/metabolism ; Neoplasm Metastasis ; Neoplasm Transplantation ; Oligonucleotide Array Sequence Analysis ; PPAR gamma/agonists ; PPAR gamma/metabolism ; Paracrine Communication ; Rosiglitazone/pharmacology ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology ; Stromal Cells/metabolism ; T-Lymphocytes/cytology
Chemical Substances	Angiogenesis Inducing Agents ; PPAR gamma ; Rosiglitazone (05V02F2KDG)
Language	English
Publishing date	2018-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-18-0912
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Article: In vivo Effects in Melanoma of ROCK Inhibition-Induced FasL Overexpression.

Teiti, Iotefa / Florie, Bertrand / Pich, Christine / Gence, Rémi / Lajoie-Mazenc, Isabelle / Rochaix, Philippe / Favre, Gilles / Tilkin-Mariamé, Anne-Françoise

Frontiers in oncology

2015 Volume 5, Page(s) 156

Abstract: Ectopic Fas-ligand (FasL) expression in tumor cells is responsible for both tumor escape through tumor counterattack of Fas-positive infiltrating lymphocytes and tumor rejection though inflammatory and immune responses. We have previously shown that RhoA ...

Abstract	Ectopic Fas-ligand (FasL) expression in tumor cells is responsible for both tumor escape through tumor counterattack of Fas-positive infiltrating lymphocytes and tumor rejection though inflammatory and immune responses. We have previously shown that RhoA GTPase and its effector ROCK negatively control FasL membrane expression in murine melanoma B16F10 cells. In this study, we found that B16F10 treatment with the ROCK inhibitor H1152 reduced melanoma development in vivo through FasL membrane overexpression. Although H1152 treatment did not reduce tumor growth in vitro, pretreatment of tumor cells with this inhibitor delayed tumor appearance, and slowed tumor growth in C57BL/6 immunocompetent mice. Thanks to the use of mice-bearing mutated Fas receptors (B6/lpr), we found that reduced tumor growth, observed in immunocompetent mice, was linked to FasL overexpression induced by H1152 treatment. Tumor growth analysis in immunosuppressed NUDE and IFN-γ-KO mice highlighted major roles for T lymphocytes and IFN-γ in the H1152-induced tumor growth reduction. Histological analyses of subcutaneous tumors, obtained from untreated versus H1152-treated B16F10 cells, showed that H1152 pretreatment induced a strong intratumoral infiltration of leukocytes. Cytofluorometric analysis showed that among these leukocytes, the number of activated CD8 lymphocytes was increased. Moreover, their antibody-induced depletion highlighted their main responsibility in tumor growth reduction. Subcutaneous tumor growth was also reduced by repeated intravenous injections of a clinical ROCK inhibitor, Fasudil. Finally, H1152-induced ROCK inhibition also reduced pulmonary metastasis implantation independently of T cell-mediated immune response. Altogether, our data suggest that ROCK inhibitors could become interesting pharmacological molecules for melanoma immunotherapy.
Language	English
Publishing date	2015-07-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2015.00156
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