LECT 2 Antagonizes FOXM1 Signaling via Inhibiting MET to Retard PDAC Progression.
FOXM1 signaling
HGF/MET
LECT2
PDAC
tumor growth
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2021
2021
Historique:
received:
30
01
2021
accepted:
30
03
2021
entrez:
3
5
2021
pubmed:
4
5
2021
medline:
4
5
2021
Statut:
epublish
Résumé
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with minimally effective treatments, highlighting the importance of developing novel biomarkers and therapeutic targets. Here, we disclosed the mechanisms that leukocyte cell-derived chemotaxin-2 (LECT2) modulates PDAC development using in vitro and in vivo models. LECT2 is downregulated in metastatic PDACs compared with the primary tumor, and its expression is correlated with multiple clinical pathologic features and prognosis. The absence promotes multiple malignant behaviors, including cell proliferation, epithelial-mesenchymal transition, migration, and invasion. In vivo studies showed that LECT2 overexpression inhibits tumor growth and lung metastasis. Mechanistically, LECT2 inhibits FOXM1 signaling by targeting HGF/MET to retard PDAC progression, revealing LECT2 as a promising biomarker and therapeutic target for PDAC in the future.
Identifiants
pubmed: 33937262
doi: 10.3389/fcell.2021.661122
pmc: PMC8082113
doi:
Types de publication
Journal Article
Langues
eng
Pagination
661122Informations de copyright
Copyright © 2021 Li, Lin, Tao, Jiang, Li, Wang, Wang and Cao.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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