S100A9 promotes the proliferation and migration of cervical cancer cells by inducing epithelialmesenchymal transition and activating the Wnt/ßcatenin pathway.
Int J Oncol
; 55(1): 35-44, 2019 Jul.
Article
en En
| MEDLINE
| ID: mdl-31059008
ABSTRACT
S100 calciumbinding protein A9 (S100A9), a member of the S100 protein family, is often upregulated in various cancers, including cervical cancer. Elevated S100A9 expression is thought to serve an important role in tumorigenesis; however, the exact role of S100A9 in the modulation of cervical cancer and the underlying molecular mechanism remain unknown. In the present study, we aimed to investigate the effects of S100A9 on the proliferation and migration of cervical cancer cells, as well as the molecular mechanisms underlying these effects. Our results demonstrated that endogenous expression of S100A9 in SiHa and CaSki cell lines was significantly higher than in the HeLa cell line. As expected, overexpression of S100A9 enhanced the proliferation and migration of cervical cancer cells. In addition, S100A9 overexpression induced epithelialmesenchymal transition (EMT) as determined by reduced expression levels of the epithelial marker Ecadherin, whereas the expression levels of the mesenchymal marker vimentin were upregulated. Furthermore, it was reported that the effects of S100A9 in the modulation of cervical cancer cells were mediated through the Wnt/ßcatenin signaling pathway as ßcatenin knockdown significantly suppressed the ability of S100A9 to enhance the proliferation and migration of cervical cancer cells. Collectively, these findings suggest that S100A9 promoted the proliferation and migration of cervical cancer cell lines. Furthermore, the underlying molecular mechanisms may be partially attributed to the induction of EMT and activation of the Wnt/ßcatenin signaling pathway.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Regulación hacia Arriba
/
Neoplasias del Cuello Uterino
/
Calgranulina B
Límite:
Female
/
Humans
Idioma:
En
Revista:
Int J Oncol
Asunto de la revista:
NEOPLASIAS
Año:
2019
Tipo del documento:
Article