Targeting PTPRK-RSPO3 colon tumours promotes differentiation and loss of stem-cell function.
Nature
; 529(7584): 97-100, 2016 Jan 07.
Article
en En
| MEDLINE
| ID: mdl-26700806
ABSTRACT
Colorectal cancer remains a major unmet medical need, prompting large-scale genomics efforts in the field to identify molecular drivers for which targeted therapies might be developed. We previously reported the identification of recurrent translocations in R-spondin genes present in a subset of colorectal tumours. Here we show that targeting RSPO3 in PTPRK-RSPO3-fusion-positive human tumour xenografts inhibits tumour growth and promotes differentiation. Notably, genes expressed in the stem-cell compartment of the intestine were among those most sensitive to anti-RSPO3 treatment. This observation, combined with functional assays, suggests that a stem-cell compartment drives PTPRK-RSPO3 colorectal tumour growth and indicates that the therapeutic targeting of stem-cell properties within tumours may be a clinically relevant approach for the treatment of colorectal tumours.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Células Madre Neoplásicas
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Neoplasias Colorrectales
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Diferenciación Celular
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Trombospondinas
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Proteínas Tirosina Fosfatasas Clase 2 Similares a Receptores
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Terapia Molecular Dirigida
Límite:
Animals
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Female
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Humans
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Male
Idioma:
En
Revista:
Nature
Año:
2016
Tipo del documento:
Article
País de afiliación:
Estados Unidos