Activation of NF-κB by TOPK upregulates Snail/Slug expression in TGF-ß1 signaling to induce epithelial-mesenchymal transition and invasion of breast cancer cells.
Biochem Biophys Res Commun
; 530(1): 122-129, 2020 09 10.
Article
en En
| MEDLINE
| ID: mdl-32828273
ABSTRACT
TGF-ß1 is known to induce epithelial-mesenchymal transition (EMT), which is a prerequisite for cancer cell invasion. Here we reveal that TOPK upregulates EMT and invasion of human breast cancer MDA-MB-231 or Hs578T cells via NF-κB-dependent Snail/Slug in TGF-ß1 signaling. Endogenous TOPK expression was significantly increased in response to TGF-ß1 and TOPK knockdown mitigated TGF-ß1-induced breast cancer cell invasion. Interestingly, TOPK knockdown restored TGF-ß1 suppression of E-cadherin expression and markedly reduced N-cadherin induced by TGF-ß1. Also, NF-κB activity or expression of EMT markers Snail and Slug induced by TGF-ß1 was decreased by TOPK knockdown. Meanwhile, knockdown of Snail or TOPK attenuated TGF-ß1-induced breast cancer cell invasion. Taken, we conclude that TOPK mediates TGF-ß1-induced EMT and invasion in breast cancer cells via NF-κB/Snail signaling, suggesting novel role of TOPK as therapeutic target in TGF-ß1-mediated breast cancer development.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Neoplasias de la Mama
/
FN-kappa B
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Quinasas de Proteína Quinasa Activadas por Mitógenos
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Factor de Crecimiento Transformador beta1
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Factores de Transcripción de la Familia Snail
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Invasividad Neoplásica
Límite:
Female
/
Humans
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
2020
Tipo del documento:
Article
País de afiliación:
Corea del Sur