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Updated: Jun 22, 2026

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice
10:13

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

Axin induces cell death and reduces cell proliferation in astrocytoma by activating the p53 pathway

Li-Ying Zhang1, Jing Ye, Feng Zhang

  • 1State Key Laboratory of Cancer Biology and Department of Pathology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, P.R. China.

International Journal of Oncology
|June 11, 2009
PubMed

Insights

Axin, a tumor suppressor, inhibits astrocytoma progression by promoting cell death and reducing proliferation, partly through the p53 pathway. Lower Axin levels correlate with higher tumor grades.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Astrocytic tumors are common brain neoplasms with diverse genetic alterations.
  • Axin functions as a tumor suppressor, regulating cell death and growth.
  • Axin interacts with p53, modulating the p53 pathway's activity.

Purpose of the Study:

  • To investigate the impact of Axin on astrocytoma progression.
  • To analyze Axin expression in astrocytoma tissues.
  • To determine Axin's effect on cell death, proliferation, and the p53 pathway in astrocytoma cells.

Main Methods:

  • Immunohistochemistry used to assess Axin expression in 96 astrocytoma cases.
  • Evaluation of apoptotic index, proliferation (Ki-67), and p53 pathway genes (p53, p21, Cyclin D1) in C6 astrocytoma cells.
  • Experimental manipulation of Axin levels (overexpression and silencing) and use of a p53 inhibitor (pifithrin-alpha).

Main Results:

  • Axin expression inversely correlated with astrocytoma grade (R=-0.286, P<0.05) and Ki-67 labeling index (R=-0.227, P<0.05).
  • Axin overexpression in C6 cells increased cell death, decreased proliferation, and upregulated p53.
  • Axin silencing reduced p53 expression; pifithrin-alpha counteracted Axin's effects.

Conclusions:

  • Axin expression is negatively associated with astrocytoma progression.
  • Axin induces apoptosis and inhibits proliferation in astrocytoma cells, partly via p53 pathway activation.
  • Understanding Axin's role provides insights into astrocytoma development and potential therapeutic strategies.

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