MAML1 regulates EMT markers expression through NOTCH-independent pathway in breast cancer cell line MCF7.
Antigens, CD
/ metabolism
Biomarkers
/ metabolism
Breast Neoplasms
/ metabolism
Cadherins
/ metabolism
Cell Line, Tumor
Cell Movement
DNA-Binding Proteins
/ antagonists & inhibitors
Epithelial-Mesenchymal Transition
Female
Humans
MCF-7 Cells
Receptors, Notch
/ metabolism
Signal Transduction
Transcription Factors
/ antagonists & inhibitors
Breast cancer
EMT
MAML1
Migration
Q real-time PCR
γ secretase inhibitor
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:
12 03 2019
12 03 2019
Historique:
received:
29
12
2018
revised:
17
01
2019
accepted:
23
01
2019
pubmed:
9
2
2019
medline:
5
11
2019
entrez:
9
2
2019
Statut:
ppublish
Résumé
Tumor relapse is the main cause of breast cancer related deaths and metastasis due to epithelial-mesenchymal transition (EMT) having a critical role in this process. MAML1 is the main co activator of NOTCH signaling pathway and its role in EMT remains unknown. In this study, this role was evaluated through overexpression and knockdown study of MAML1 in MCF7 and MDA-MB-231 cells. MAML1 overexpression up regulated the epithelial and down regulated the mesenchymal markers. In addition, MAML1 silencing decreased epithelial and increased mesenchymal markers. Notch inhibition using γ-secretase inhibitor resulted in increased E-cadherin expression. MAML1 ectopic expression, further increased E-cadherin expression with inhibition of NOTCH signaling. Wound healing assay showed that MAML1 overexpression decreases the rate of migration, while MAML1 silencing increases this rate significantly. In conclusion, our data indicated that MAML1 negatively regulates EMT markers expression in breast cancer cells.
Identifiants
pubmed: 30732857
pii: S0006-291X(19)30125-1
doi: 10.1016/j.bbrc.2019.01.101
pii:
doi:
Substances chimiques
Antigens, CD
0
Biomarkers
0
CDH1 protein, human
0
Cadherins
0
DNA-Binding Proteins
0
MAML1 protein, human
0
Receptors, Notch
0
Transcription Factors
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
376-382Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.