FEBS Letters
Volume 584, Issue 18 , Pages 4097-4101, 24 September 2010

Knockdown of apoptosis signal-regulating kinase 1 modulates basal glycogen synthase kinase-3β kinase activity and regulates cell migration

Edited by Gianni Cesareni

  • Kyung Tae Noh

      Affiliations

    • Laboratories of Cell Death and Human Diseases, School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Republic of Korea
    • ,
  • Ssang-Goo Cho

      Affiliations

    • Department of Animal Biotechnology, Konkuk University, Seoul 143-701, Republic of Korea
    • ,
  • Eui-Ju Choi

      Affiliations

    • Laboratories of Cell Death and Human Diseases, School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Republic of Korea
    • Corresponding Author InformationCorresponding author. Fax: +82 2 3290 4741.

Received 14 July 2010; received in revised form 11 August 2010; accepted 18 August 2010. published online 26 August 2010.

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.

Keywords: ASK1, GSK-3β, β-Catenin, Axin, Migration

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PII: S0014-5793(10)00690-3

doi:10.1016/j.febslet.2010.08.029

FEBS Letters
Volume 584, Issue 18 , Pages 4097-4101, 24 September 2010

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