NFIC1 suppresses migration and invasion of breast cancer cells through interferon-mediated Jak-STAT pathway.
Arch Biochem Biophys
; 727: 109346, 2022 09 30.
Article
em En
| MEDLINE
| ID: mdl-35798053
ABSTRACT
NFIC1, the longest isoform of NFIC, is essential for the regulation on spatiotemporal expression of drug-metabolizing genes in liver. However, the role of NFIC1 in breast cancer is not clear. Here we showed that increased expression of NFIC1 suppressed the migration and invasion of MCF-7 cells. NFIC1 overexpression increased the expression of IFNB1, IFNL1, IFNL2 and IFNL3, and the activation of interferon-mediated Jak-STAT pathway was enhanced by NFIC1 overexpression. Treatment with Jak-STAT pathway inhibitors, Filgotinib or Ruxolitinib, reversed the suppressive effects of NFIC1 overexpression on migration and invasion of MCF-7 cells. In addition, we found that MX1 and MX2, two target genes of Jak-STAT pathway, mediated the migration and invasion of MCF-7 cells. These results demonstrated that NFIC1 inhibited the migration and invasion in MCF-7 cells through interferon-mediated activation of Jak-STAT pathway, indicating that Jak-STAT pathway might be a potential therapeutic target for preventing breast cancer metastasis.
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Base de dados:
MEDLINE
Assunto principal:
Neoplasias da Mama
/
Fatores de Transcrição NFI
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Janus Quinases
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article