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Inhibition of RAC1 activity in cancer associated fibroblasts favours breast tumour development through IL-1ß upregulation.
Martínez-López, Angélica; García-Casas, Ana; Bragado, Paloma; Orimo, Akira; Castañeda-Saucedo, Eduardo; Castillo-Lluva, Sonia.
Afiliação
  • Martínez-López A; Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Biológicas, Universidad Complutense, Madrid, 28040, Spain; Laboratorio de Biología Celular del Cáncer, Facultad de Ciencias Químico-Biológicas, Universidad Autónoma de Guerrero, Mexico.
  • García-Casas A; Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Biológicas, Universidad Complutense, Madrid, 28040, Spain; Instituto de Investigaciones Sanitarias San Carlos (IdISSC), Madrid, 28040, Spain.
  • Bragado P; Instituto de Investigaciones Sanitarias San Carlos (IdISSC), Madrid, 28040, Spain; Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense, Madrid, 28040, Spain.
  • Orimo A; Department of Pathology and Oncology, Juntendo University School of Medicine, Tokyo, Japan.
  • Castañeda-Saucedo E; Laboratorio de Biología Celular del Cáncer, Facultad de Ciencias Químico-Biológicas, Universidad Autónoma de Guerrero, Mexico.
  • Castillo-Lluva S; Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Biológicas, Universidad Complutense, Madrid, 28040, Spain; Instituto de Investigaciones Sanitarias San Carlos (IdISSC), Madrid, 28040, Spain. Electronic address: sonica01@ucm.es.
Cancer Lett ; 521: 14-28, 2021 Aug 19.
Article em En | MEDLINE | ID: mdl-34419498
Cancer-associated fibroblasts (CAFs) are highly abundant stromal components in the tumour microenvironment. These cells contribute to tumorigenesis and indeed, they have been proposed as a target for anti-cancer therapies. Similarly, targeting the Rho-GTPase RAC1 has also been suggested as a potential therapeutic target in cancer. Here, we show that targeting RAC1 activity, either pharmacologically or by genetic silencing, increases the pro-tumorigenic activity of CAFs by upregulating IL-1ß secretion. Moreover, inhibiting RAC1 activity shifts the CAF subtype to a more aggressive phenotype. Thus, as RAC1 suppresses the secretion of IL-1ß by CAFs, reducing RAC1 activity in combination with the depletion of this cytokine should be considered as an interesting therapeutic option for breast cancer in which tumour cells retain intact IL-1ß signalling.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Risk_factors_studies Idioma: En Revista: Cancer Lett Ano de publicação: 2021 Tipo de documento: Article País de afiliação: México País de publicação: Irlanda

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Risk_factors_studies Idioma: En Revista: Cancer Lett Ano de publicação: 2021 Tipo de documento: Article País de afiliação: México País de publicação: Irlanda