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TWIST interacts with β-catenin signaling on osteosarcoma cell survival against cisplatin

Jianhuang Wu1, Qiande Liao, Hongbo He

  • 1Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Spine, Xiangya Hospital, Central South University, Changsha, Hunan, China.

Molecular Carcinogenesis
|January 3, 2013
PubMed

Insights

TWIST reduces osteosarcoma cell survival against cisplatin by decreasing soluble β-catenin levels via PI3K signaling. This reveals a novel functional link between TWIST and β-catenin in osteosarcoma development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • TWIST and Wnt/β-catenin signaling are implicated in osteosarcoma.
  • Understanding their interaction is crucial for therapeutic strategies.

Purpose of the Study:

  • To investigate TWIST's regulation of β-catenin in osteosarcoma cells.
  • To determine the impact of TWIST-β-catenin interaction on cisplatin resistance.

Main Methods:

  • TWIST overexpression in Saos-2 cells and knockdown in MG-63 cells.
  • Assessed soluble β-catenin levels, GSK-3β phosphorylation, and target gene expression.
  • Evaluated cell survival against cisplatin, with and without β-catenin or PI3K inhibition.

Main Results:

  • TWIST overexpression decreased soluble β-catenin, GSK-3β phosphorylation, target gene expression, and cisplatin resistance.
  • TWIST knockdown increased soluble β-catenin, GSK-3β phosphorylation, target gene expression, and cisplatin resistance.
  • TWIST's effects were mediated by PI3K signaling and linked to β-catenin levels.

Conclusions:

  • TWIST diminishes osteosarcoma cell survival against cisplatin by reducing soluble β-catenin through a PI3K-dependent pathway.
  • This study establishes a functional link between TWIST and β-catenin signaling in osteosarcoma.
  • Provides new insights into osteosarcoma molecular mechanisms and potential therapeutic targets.
Keywords:
TWISTcell survivalcisplatinosteosarcomaβ-catenin

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