Abstract
Backgroundδ-Catenin (CTNND2), which encodes a scaffold protein in humans, has been found in a few malignancies. However, the expression pattern and contribution of δ-catenin to astrocytoma progression are unclear.MethodsWe investigated δ-catenin expression in human astrocytoma samples and its function in astrocytoma cell lines using immunohistochemistry, siRNA knockdown, transfection, MTT, transwell migration and Rac1 pulldown techniques.Resultsδ-Catenin protein expression was detected in cytoplasm of astrocytoma cells by immunohistochemistry. Analysis showed that grade I astrocytoma (0%, 0/11) and glial cells from normal brain tissue exhibited negative staining. δ-Catenin expression was significantly higher in grade III-IV (35%, 29/84) compared to grade II astrocytoma cells (18%, 11/61); p < 0.01). In addition, CTNND2 overexpression promoted proliferation, invasion and Rac1 activity of U251 astrocytoma cells. Treatment of δ-catenin-transfected cells with a Rac1 inhibitor decreased Rac1 activity and invasion. δ-Catenin knockdown in U87 glioblastoma cell decreased cell proliferation, invasion and Rac1 activity.ConclusionThe results suggest that δ-catenin expression is associated with the malignant progression of astrocytoma and promotes astrocytoma cell invasion through upregulation of Rac1 activity. δ-Catenin expression levels may serve as a useful marker of the biological behavior of astrocytoma cells.
Highlights
Astrocytoma arises from neural stem or progenitor cells in the central nervous system
We investigated the effect of δ-catenin on Rac1 activity and the biological behavior of astrocytoma cell lines
The histological diagnosis and differentiation grade were evaluated for sections stained with hematoxylin and eosin according to the World Health Organization (WHO) classification guidelines
Summary
Astrocytoma arises from neural stem or progenitor cells in the central nervous system. It is the most common primary brain tumor and accounts for approximately 60% of all brain tumors. Despite combined treatment strategies, which include surgery, radiotherapy and chemotherapy, the prognosis for high-grade astrocytoma, especially glioblastoma multiforme, has changed little over the past 10 years, with a median survival of only approximately 1 year [1]. The histological grade partly reflects the malignant features of astrocytoma, it cannot give an indication of the exact mechanism of tumor invasion and recurrence [2,3]. It is important to understand the molecular mechanism of astrocytoma cell invasion and identify effective markers in tumorigenesis and progression
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