Limb-bud and heart (LBH) inhibits cellular migration, invasion and epithelial-mesenchymal transition in nasopharyngeal carcinoma via downregulating αB-crystallin expression.
Animals
Cell Line, Tumor
Cell Movement
/ genetics
Crystallins
/ genetics
Epithelial-Mesenchymal Transition
/ genetics
Gene Expression Regulation, Neoplastic
Humans
Nasopharyngeal Carcinoma
/ pathology
Nasopharyngeal Neoplasms
/ genetics
Neoplasm Invasiveness
/ genetics
Transcription Factors
/ metabolism
alpha-Crystallin B Chain
EMT process
LBH
Migration
Nasopharyngeal carcinoma
αB-crystallin
Journal
Cellular signalling
ISSN: 1873-3913
Titre abrégé: Cell Signal
Pays: England
ID NLM: 8904683
Informations de publication
Date de publication:
09 2021
09 2021
Historique:
received:
31
12
2020
revised:
06
04
2021
accepted:
12
05
2021
pubmed:
18
5
2021
medline:
1
4
2022
entrez:
17
5
2021
Statut:
ppublish
Résumé
Limb-bud and heart (LBH) gene has received increasing attention in recent cancer studies. Here we investigated the role of the LBH gene in regulating the metastasis capacity and epithelial-mesenchymal transition (EMT) of nasopharyngeal carcinoma (NPC) cells, and its potential mechanism. The expressions of LBH and αB-crystallin (CRYAB) were modulated by lentiviral infection, or plasmid/siRNA transfection, and the phosphorylation of p38 was suppressed by an inhibitor, to explore their functions in modulating NPC cell phenotypes, as well as the relationships of these factors with each other. Cellular proliferation, migration and invasion were examined by RTCA system, Transwell assays and Matrigel Transwell assays respectively. The EMT progression was indicated by RT-qPCR and Western blotting measuring the expressions of EMT biomarkers. NPC xenografts were constrcucted, and formed tumors were sectioned for morphology and immunohistofluorescence. The interaction between LBH and CRYAB was examined by colocalization and Fluorescence resonance energy transfer (FRET) analysis. We reached the conclusion that LBH inhibits the proliferation, migration, invasion and EMT of NPC cells, and its effects were partially achieved by suppressing p38 phosphorylation, which subsequently downregulates the mRNA expression and phosphorylation of CRYAB, while CRYAB directly interacts with LBH in NPC cells. This LBH-related pathway we revealed provides a novel therapeutic target for nasopharyngeal carcinoma research.
Identifiants
pubmed: 34000384
pii: S0898-6568(21)00134-0
doi: 10.1016/j.cellsig.2021.110045
pii:
doi:
Substances chimiques
CRYAB protein, human
0
Crystallins
0
LBH protein, human
0
Transcription Factors
0
alpha-Crystallin B Chain
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
110045Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.