BTF3 promotes stemness and inhibits TypeⅠInterferon signaling pathway in triple-negative breast cancer.
Cell Line, Tumor
Cell Movement
/ genetics
Cell Proliferation
/ genetics
Female
Gene Expression Regulation, Neoplastic
Humans
Interferon Regulatory Factor-7
/ genetics
Interferon Type I
/ metabolism
Neoplastic Stem Cells
/ metabolism
Nuclear Proteins
/ metabolism
Phenotype
Polycomb Repressive Complex 1
/ metabolism
Protein Biosynthesis
RNA, Messenger
/ genetics
Signal Transduction
Transcription Factors
/ metabolism
Treatment Outcome
Triple Negative Breast Neoplasms
/ genetics
BTF3
IRF7
Interferon signaling pathway
Stemness
Triple-negative breast cancer
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
22 01 2021
22 01 2021
Historique:
received:
17
12
2020
accepted:
17
12
2020
pubmed:
1
1
2021
medline:
23
4
2021
entrez:
31
12
2020
Statut:
ppublish
Résumé
Triple-negative breast cancer (TNBC) is a major challenge in clinical practice due to its aggressiveness and lack of targeted treatment. Cancer stem-like traits contribute to tumorigenesis and immune privilege of TNBC. However, the relationship of stemness and immunosurveillance remains unclear. Here, we demonstrate that BTF3 expression is related with stem-like properties in TNBC cells. BTF3 modulates stemness, migration and proliferation of TNBC in vitro. Bioinformatics analysis revealed that interferon signaling pathways and IRF7, both of which participate in the immune escape of TNBC, are closely related to BTF3 in TNBC cells. Knockdown of BTF3 activates IRF7 expression through increased degradation of BMI1, a protein that can represses IRF7 transcription by directly binding to its promotor region. BTF3 links stem-like traits and the interferon signaling pathway, revealing the potential connection of stemness and immunomodulation in TNBC. Clinically, we suggest that BTF3 is predictive of poor prognosis in patients with TNBC. Together, our findings highlight an important role of BTF3 in regulating the progression of TNBC cells.
Identifiants
pubmed: 33383560
pii: S0006-291X(20)32237-3
doi: 10.1016/j.bbrc.2020.12.060
pii:
doi:
Substances chimiques
BMI1 protein, human
0
IRF7 protein, human
0
Interferon Regulatory Factor-7
0
Interferon Type I
0
Nuclear Proteins
0
RNA, Messenger
0
Transcription Factors
0
transcription factor BTF3
0
Polycomb Repressive Complex 1
EC 2.3.2.27
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
22-28Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare no conflict of interest.