S100B promotes chemoresistance in ovarian cancer stem cells by regulating p53.
Oncol Rep
; 40(3): 1574-1582, 2018 Sep.
Article
en En
| MEDLINE
| ID: mdl-29956807
ABSTRACT
Chemoresistance is one of the most important causes of ovarian cancerrelated deaths. Recently, cancer stem cells (CSCs) have been recognized as the source of chemoresistance in ovarian cancer. However, the underlying mechanisms that regulate the chemoresistance of ovarian CSCs (OCSCs) remain unclear. The aim of the present study was to investigate the roles of S100B in the regulation of OCSC chemoresistance, which provides a novel therapeutic target. We observed high expression of S100B in CD133+ OCSCs derived from ovarian cancer cell lines and primary tumors and in cisplatinresistant patient samples. Then, we determined that S100B knockdown promoted the apoptosis of OCSCs after treatment with different concentrations of cisplatin. The underlying mechanism of S100Bmediated chemoresistance in OCSCs may be through p53 inhibition. Furthermore, drugresistance genes, including MDR1 and MRP1, were involved in the process of S100Bmediated OCSC chemoresistance. In conclusion, our results elucidated the importance of S100B in the maintenance of OCSC chemoresistance, which may provide a promising therapeutic target for ovarian cancer.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neoplasias Ováricas
/
Células Madre Neoplásicas
/
Biomarcadores de Tumor
/
Proteína p53 Supresora de Tumor
/
Cistadenocarcinoma Seroso
/
Resistencia a Antineoplásicos
/
Subunidad beta de la Proteína de Unión al Calcio S100
Tipo de estudio:
Prognostic_studies
Límite:
Female
/
Humans
/
Middle aged
Idioma:
En
Revista:
Oncol Rep
Asunto de la revista:
NEOPLASIAS
Año:
2018
Tipo del documento:
Article