Selective hemangioma cell dysfunction and apoptosis triggered by in vitro treatment with imiquimod

Infantile hemangiomas are the most common benign tumors of infancy, characterized by unregulated angiogenesis and endothelial cells with high mitotic rate. Although spontaneous regression occurs, sometimes treatment is required and alternatives to corticosteroids should be considered to reduce side...

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Autor principal: Rocco, R.
Otros Autores: Alegre, N., Pozner, R., Wainstok, Rosa, Gazzaniga, S.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: Elsevier Ireland Ltd 2018
Acceso en línea:Registro en Scopus
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Registro en la Biblioteca Digital
Aporte de:Registro referencial: Solicitar el recurso aquí
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024 7 |2 scopus  |a 2-s2.0-85042352134 
024 7 |2 cas  |a imiquimod, 99011-02-6; Aminoquinolines; Antineoplastic Agents; imiquimod 
030 |a TOLED 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
100 1 |a Rocco, R. 
245 1 0 |a Selective hemangioma cell dysfunction and apoptosis triggered by in vitro treatment with imiquimod 
260 |b Elsevier Ireland Ltd  |c 2018 
270 1 0 |m Gazzaniga, S.; Laboratorio de Biología Tumoral, Dpto. de Química Biológica IQUIBICEN-CONICET, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos AiresArgentina; email: sgazza@qb.fcen.uba.ar 
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504 |a Sapijaszko, M.J., Imiquimod 5% cream (Aldara) in the treatment of basal cell carcinoma (2005) Skin Ther. Lett., 10, pp. 2-5 
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504 |a Jiang, C., Hu, X., Ma, G., A prospective self-controlled phase II study of imiquimod 5% cream in the treatment of infantile hemangioma (2011) Pediatr. Dermatol., 28, pp. 259-266 
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506 |2 openaire  |e Política editorial 
520 3 |a Infantile hemangiomas are the most common benign tumors of infancy, characterized by unregulated angiogenesis and endothelial cells with high mitotic rate. Although spontaneous regression occurs, sometimes treatment is required and alternatives to corticosteroids should be considered to reduce side effects. Imiquimod is an imidazoquinoline, approved for some skin pathologies other than hemangioma. It is proposed that the effectiveness of imiquimod comes from the activation of immune cells at tumor microenvironment. However, the possibility to selectively kill different cell types and to directly impede angiogenesis has been scarcely explored in vitro for endothelial cells. In this work we showed a dramatic cytotoxicity on hemangioma cell, with a significant lower IC50 value in hemangioma compared to normal endothelial cells and melanoma (employed as a non-endothelial tumor cell line). Nuclear morphometric and flow-cytometry assays revealed imiquimod-induced apoptosis on hemangioma and melanoma cells but a small percentage of senescence on normal endothelial cells. At sub-lethal conditions, cell migration, a key step in angiogenesis turned out to be inhibited in a tumor-selective manner along with actin cytoskeleton disorganization on hemangioma cells. Altogether, these findings pointed out the selective cytotoxic effects of imiquimod on transformed endothelial cells, evidencing the potential for imiquimod to be a therapeutic alternative to reduce extensive superficial hemangioma lesions. © 2018 Elsevier B.V.  |l eng 
536 |a Detalles de la financiación: Secretaría de Ciencia y Técnica, Universidad de Buenos Aires, 20020130200082BA 
536 |a Detalles de la financiación: This work was supported by grants from CONICET and University of Buenos Aires, UBACYT 20020130200082BA . We would like to thank Dr. Adriana Cochón for providing assistance in statistical analysis of cytotoxicity assays. Appendix A 
593 |a Laboratorio de Biología Tumoral, Dpto. de Química Biológica IQUIBICEN-CONICET, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina 
593 |a Institute of Experimental Medicine (IMEX) -CONICET, National Academy of Medicine, Buenos Aires, Argentina 
690 1 0 |a CYTOTOXICITY 
690 1 0 |a ENDOTHELIUM 
690 1 0 |a HEMANGIOMA 
690 1 0 |a IMIQUIMOD 
690 1 0 |a IMIQUIMOD 
690 1 0 |a AMINOQUINOLINE DERIVATIVE 
690 1 0 |a ANTINEOPLASTIC AGENT 
690 1 0 |a IMIQUIMOD 
690 1 0 |a ACTIN FILAMENT 
690 1 0 |a ANGIOGENESIS 
690 1 0 |a ANIMAL CELL 
690 1 0 |a APOPTOSIS 
690 1 0 |a ARTICLE 
690 1 0 |a CAPILLARY HEMANGIOMA 
690 1 0 |a CELL MIGRATION 
690 1 0 |a CELL TRANSFORMATION 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DRUG CYTOTOXICITY 
690 1 0 |a DRUG SELECTIVITY 
690 1 0 |a ENDOTHELIUM CELL 
690 1 0 |a FLOW CYTOMETRY 
690 1 0 |a HEMANGIOMA CELL 
690 1 0 |a IC50 
690 1 0 |a IMMUNOCOMPETENT CELL 
690 1 0 |a IMMUNOSTIMULATION 
690 1 0 |a IN VITRO STUDY 
690 1 0 |a MELANOMA CELL LINE 
690 1 0 |a MORPHOMETRY 
690 1 0 |a MOUSE 
690 1 0 |a NONHUMAN 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a STRESS FIBER 
690 1 0 |a TUMOR CELL 
690 1 0 |a TUMOR MICROENVIRONMENT 
690 1 0 |a ANIMAL 
690 1 0 |a APOPTOSIS 
690 1 0 |a CELL AGING 
690 1 0 |a CELL MOTION 
690 1 0 |a CELL NUCLEUS 
690 1 0 |a CELL SURVIVAL 
690 1 0 |a CYTOSKELETON 
690 1 0 |a DRUG EFFECTS 
690 1 0 |a EXPERIMENTAL MELANOMA 
690 1 0 |a HEMANGIOMA 
690 1 0 |a HUMAN 
690 1 0 |a PATHOLOGY 
690 1 0 |a SKIN TUMOR 
690 1 0 |a TUMOR CELL LINE 
690 1 0 |a ULTRASTRUCTURE 
690 1 0 |a AMINOQUINOLINES 
690 1 0 |a ANIMALS 
690 1 0 |a ANTINEOPLASTIC AGENTS 
690 1 0 |a APOPTOSIS 
690 1 0 |a CELL LINE, TUMOR 
690 1 0 |a CELL MOVEMENT 
690 1 0 |a CELL NUCLEUS 
690 1 0 |a CELL SURVIVAL 
690 1 0 |a CELLULAR SENESCENCE 
690 1 0 |a CYTOSKELETON 
690 1 0 |a ENDOTHELIAL CELLS 
690 1 0 |a HEMANGIOMA 
690 1 0 |a HUMANS 
690 1 0 |a MELANOMA, EXPERIMENTAL 
690 1 0 |a MICE 
690 1 0 |a SKIN NEOPLASMS 
690 1 0 |a STRESS FIBERS 
700 1 |a Alegre, N. 
700 1 |a Pozner, R. 
700 1 |a Wainstok, Rosa 
700 1 |a Gazzaniga, S. 
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