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β-Catenin Signalling in Glioblastoma Multiforme and Glioma-Initiating Cells

机译：胶质母细胞瘤和胶质瘤起始细胞中的β-连环蛋白信号传导

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摘要

Glioblastoma multiforme (GBM) is a commonly occurring brain tumor with a poor prognosis. GBM can develop both “de novo” or evolve from a previous astrocytoma and is characterized by high proliferation and infiltration into the surrounding tissue. Following treatment (surgery, radiotherapy, and chemotherapy), tumors often reappear. Glioma-initiating cells (GICs) have been identified in GBM and are thought to be responsible for tumors initiation, their continued growth, and recurrence.β-catenin, a component of the cell-cell adhesion complex and of the canonical Wnt pathway, regulates proliferation, adhesion, and migration in different cell types.β-catenin and components of the Wnt canonical pathway are commonly overexpressed in GBM. Here, we review previous work on the role of Wnt/β-catenin signalling in glioma initiation, proliferation, and invasion. Understanding the molecular mechanisms regulating GIC biology and glioma progression may help in identifying novel therapeutic targets for GBM treatment.
机译：多形胶质母细胞瘤（GBM）是一种常见的脑肿瘤，预后较差。 GBM可以“从头发展”或从先前的星形细胞瘤发展而来，其特征是高度增殖和向周围组织的浸润。经过治疗（手术，放疗和化疗）后，肿瘤通常会再次出现。已在GBM中鉴定出胶质瘤起始细胞（GIC），它们被认为与肿瘤的起始，它们的持续生长和复发有关.β-catenin是细胞-细胞粘附复合物和Wnt通路的组成部分，可调节β-catenin和Wnt规范途径的成分通常在GBM中过表达。在这里，我们回顾了Wnt /β-catenin信号传导在神经胶质瘤的发生，增殖和侵袭中的作用。了解调节GIC生物学和神经胶质瘤进展的分子机制可能有助于确定GBM治疗的新治疗靶标。

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