Dickkopf-1 enhances migration of HEK293 cell by beta-catenin/E-cadherin degradation

Migration is an important process during cellular activity and embryo development. We recently showed that Dickkopf-1(Dkk-1), an antagonist of Wnt/ beta-catenin signaling pathway, could promote trophoblast cell invasion during murine placentation. However, mechanism of Dkk-1 action on cell migration was not clear. The objective of this study was to further evaluate the effect of Dkk-1 on cell migration and to identify the underlining mechanisms. Functional assays with stable Dkk-1 transfected HEK293 cells revealed that Dkk-1 expression increased cell migration by decreasing cell-cell adhesion, not cell-matrix adhesion. Treatment with LiCl and Genistein (widely used inhibitor of glycogen synthase kinase-3 and tyrosine protein kinase, respectively.) could inhibit the migration effect of Dkk-1, and significantly increased the membrane localization of beta-catenin and E-cadherin in HEK293 cells transfected with Dkk-1. Further data showed that HEK293 cells transfected with Dkk-1 have significantly decreased accumulation of both beta-catenin and E-cadherin at the cell membrane. Together, our data suggest that Dkk-1 stimulates the release of beta-catenin from cell membrane and facilitates cell migration which accompanies degradation of beta-catenin/E-cadherin.

Medienart:

E-Artikel

Erscheinungsjahr:

2009

Erschienen:

2009

Enthalten in:

Zur Gesamtaufnahme - volume:14

Enthalten in:

Frontiers in bioscience (Landmark edition) - 14(2009), 6 vom: 01. Jan., Seite 2212-20

Sprache:

Englisch

Beteiligte Personen:

Kuang, Hai-Bin [VerfasserIn]
Miao, Cheng-Lin [VerfasserIn]
Guo, Wei-Xiang [VerfasserIn]
Peng, Sha [VerfasserIn]
Cao, Yu-Jing [VerfasserIn]
Duan, En-Kui [VerfasserIn]

Links:

Volltext

Themen:

Beta Catenin
Cadherins
DH2M523P0H
DKK1 protein, human
G4962QA067
Genistein
Intercellular Signaling Peptides and Proteins
Journal Article
Lithium Chloride
Research Support, Non-U.S. Gov't

Anmerkungen:

Date Completed 07.04.2009

Date Revised 27.02.2022

published: Electronic

Citation Status MEDLINE

doi:

10.2741/3373

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM186960670