AXIN1 Expression and Localization in Meningiomas and Association to Changes of APC and E-cadherin

Nives Pećina-Šlaus1, Anja Kafka2, Tomislav Vladušić3

  • 1Laboratory of Neurooncology, Croatian Institute for Brain Research, School of Medicine University of Zagreb, Zagreb, Croatia Department of Biology, School of Medicine, University of Zagreb, Zagreb, Croatia nina@mef.hr.

Anticancer Research
|September 16, 2016
PubMed
Abstract

Insights

Genetic alterations and altered expression of the AXIN1 tumor suppressor gene are implicated in intracranial meningiomas. These changes correlate with Wnt pathway molecules, impacting tumor development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • AXIN1 acts as a tumor suppressor by inhibiting the Wnt signaling pathway.
  • It down-regulates beta-catenin via an AXIN-based destruction complex.
  • The role of AXIN1 in intracranial meningioma remains to be fully elucidated.

Purpose of the Study:

  • To investigate the involvement of AXIN1 in intracranial meningioma.
  • To analyze genetic alterations and protein expression of AXIN1 in meningiomas.
  • To correlate AXIN1 alterations with Wnt pathway components.

Main Methods:

  • Loss of heterozygosity and microsatellite instability analyses were performed on meningioma samples.
  • Immunohistochemistry was used to assess AXIN1 protein expression and localization.
  • Statistical analyses (Chi-Square, Pearson's correlations) compared AXIN1 findings with APC, beta-catenin, and E-cadherin expression.

Main Results:

  • Allelic deletions of AXIN1 occurred in 21.1% of meningiomas; microsatellite instability in 5.3%.
  • Weak or absent AXIN1 expression was observed in 21.9% of tumors.
  • AXIN1 genetic changes correlated with lack of APC expression and presence of mutant APC proteins, and with E-cadherin expression.

Conclusions:

  • Genetic alterations and altered expression of AXIN1 are involved in meningioma pathogenesis.
  • AXIN1's relationship with specific Wnt pathway molecules, including APC and E-cadherin, is highlighted.
  • These findings provide novel insights into the molecular mechanisms of meningeal brain tumors.

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