Oncostatin M activates STAT3 to promote endometrial cancer invasion and angiogenesis.
Oncol Rep
; 34(1): 129-38, 2015 Jul.
Article
em En
| MEDLINE
| ID: mdl-25954856
ABSTRACT
Oncostatin M (OSM), a pleiotropic cytokine, can either promote or inhibit the growth of tumors derived from specific tissues. However, little is known about the activity and expression pattern of OSM in endometrial cancers (ECs). Herein we show that expression of OSM in human ECs was significantly higher than that in hyperplastic or normal tissues. In EC tissues, high OSM levels were positively correlated with tumor stage, histological grade, myometrial invasion, and lymph node metastasis. Additionally, we demonstrated that recombinant human OSM (rhOSM) promoted tumor angiogenesis in EC cell lines by activating STAT3 (signal transducer and activator of transcription 3) and enhanced both cell migration and cell invasion. rhOSM did not, however, influence the proliferation of EC cells in vitro. In contrast, in our in vivo xenograft model, overexpression of rhOSM promoted cell proliferation, tumor growth, and angiogenesis in nude mice. Collectively, these experiments suggest that OSM may be a tumor promoter that encourages EC progression. OSM may thus serve as a potential target of antiangiogenic therapy for endometrial cancer.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias do Endométrio
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Fator de Transcrição STAT3
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Oncostatina M
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Neovascularização Patológica
Tipo de estudo:
Prognostic_studies
Limite:
Animals
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Female
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Humans
Idioma:
En
Ano de publicação:
2015
Tipo de documento:
Article