Abstract
GSK-3β is a basally active kinase. Axin forms a complex with GSK-3β and β-catenin; this complex promotes the GSK-3β-dependent phosphorylation of β-catenin, thereby inducing its degradation. However, the inhibition of GSK-3β provokes cell migration via the dysregulation of β-catenin. In this study, we determined that the level of apoptosis signal-regulating kinase 1 (ASK1) was lower in a metastatic breast cancer cell line, compared to that of non-metastatic cancer cell lines and the knockdown of ASK1 not only induces β-catenin activation via the inhibition of GSK-3β and collapsing the subsequent protein complex by regulating Axin dynamics, but also stimulates cell migration. Together, the blockage of the GSK-3β-β-catenin pathway resulting from the knockdown of ASK1 modulates the migration of breast cancer cells.
| Original language | English |
|---|---|
| Pages (from-to) | 4097-4101 |
| Number of pages | 5 |
| Journal | FEBS Letters |
| Volume | 584 |
| Issue number | 18 |
| DOIs | |
| Publication status | Published - 2010 Sept |
Bibliographical note
Funding Information:We would like to thank Dr. Woo Keun Song (GIST of South Korea) for the pTopflash plasmid. This work was supported by a NRF Grant (2010-0001197), by the Original Technology Research Program for Brain Science (2010-0002153) and the Mid-career Researcher Program (2010-0000488) through NRF Grant funded by the Ministry of Education, Science & Technology (MEST) of the Korea (E.-J.C.).
Keywords
- ASK1
- Axin
- GSK-3β
- Migration
- β-Catenin
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology
