Blocking the FSTL1-DIP2A Axis Improves Anti-tumor Immunity.
Cell Rep
; 24(7): 1790-1801, 2018 08 14.
Article
em En
| MEDLINE
| ID: mdl-30110636
ABSTRACT
Immune dysfunction is a strong factor in the resistance of cancer to treatment. Blocking immune checkpoint pathways is a promising approach to improve anti-tumor immunity, but the clinical efficacies are still limited. We previously identified follistatin-like 1 (FSTL1) as a determinant of immune dysfunction mediated by mesenchymal stromal/stem cells (MSCs) and immunoregulatory cells. Here, we demonstrate that blocking FSTL1 but not immune checkpoint pathways significantly suppresses cancer progression and metastasis in several mouse tumor models with increased MSCs. Expression of DIP2A (the receptor of FSTL1) in tumor cells is critical for FSTL1-induced immunoresistance. FSTL1/DIP2A co-positivity in tumor tissues correlates with poor prognosis in NSCLC patients. Thus, breaking the FSTL1-DIP2A axis may be a useful strategy for successfully inducing anti-tumor immunity.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Nucleares
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Proteínas de Transporte
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Regulação Neoplásica da Expressão Gênica
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Carcinoma Pulmonar de Células não Pequenas
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Proteínas Relacionadas à Folistatina
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Imunidade Inata
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Neoplasias Pulmonares
Tipo de estudo:
Diagnostic_studies
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Observational_studies
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Prognostic_studies
/
Risk_factors_studies
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article