NUPR1 promotes the proliferation and migration of breast cancer cells by activating TFE3 transcription to induce autophagy.
Autophagy
Breast cancer
NUPR1
TFE3
Journal
Experimental cell research
ISSN: 1090-2422
Titre abrégé: Exp Cell Res
Pays: United States
ID NLM: 0373226
Informations de publication
Date de publication:
01 09 2022
01 09 2022
Historique:
received:
07
12
2021
revised:
25
05
2022
accepted:
28
05
2022
pubmed:
7
6
2022
medline:
20
7
2022
entrez:
6
6
2022
Statut:
ppublish
Résumé
Recurrence and metastasis affect the survival rate of breast cancer patients. The fundamental reason lies in the lack of understanding of the mechanism of breast cancer metastasis. In this study, the proliferation, migration and invasion abilities of breast cancer cells were evaluated. The mechanism of NUPR1/TFE3 signaling pathway on autophagy-related proteins and migration-invasion-related proteins was examined in cell model in vitro. The effects of NUPR1 on malignancy formation and metastasis were investigated in vivo. We found that NUPR1 was upregulated in breast cancer cells and tissues. NUPR1 knockdown inhibited the proliferation, migration and invasion of ZR-75-30 cells and inhibited malignancy formation and metastasis in vivo. Mechanically, NUPR1 promoted autophagy by activating of TFE3 transcription, thereby regulating breast cancer metastasis. This paper indicates that NUPR1 activates autophagy through the TFE3 signaling pathway to promote breast cancer metastasis, and provides a biological basis for the intervention of blocking distant metastasis.
Identifiants
pubmed: 35660538
pii: S0014-4827(22)00227-0
doi: 10.1016/j.yexcr.2022.113234
pii:
doi:
Substances chimiques
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
0
Basic Helix-Loop-Helix Transcription Factors
0
NUPR1 protein, human
0
Neoplasm Proteins
0
TFE3 protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
113234Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.