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Updated: Apr 24, 2026

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Published on: November 28, 2015
Transient axonal glycoprotein-1 induces apoptosis-related gene expression without triggering apoptosis in U251 glioma
Haigang Chang1, Shanshan Song2, Zhongcan Chen3
1Department of Neurosurgery, the First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan Province, China ; Neurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong Province, Department of Neurosurgery, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China.
Abstract:
Previous studies show that transient axonal glycoprotein-1, a ligand of amyloid precursor protein, increases the secretion of amyloid precursor protein intracellular domain and is involved in apoptosis in Alzheimer's disease. In this study, we examined the effects of transient axonal glycoprotein-1 on U251 glioma cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that transient axonal glycoprotein-1 did not inhibit the proliferation of U251 cells, but promoted cell viability. The terminal deoxynucleotidyl transferase dUTP nick end labeling assay showed that transient axonal glycoprotein-1 did not induce U251 cell apoptosis. Real-time PCR revealed that transient axonal glycoprotein-1 substantially upregulated levels of amyloid precursor protein intracellular C-terminal domain, and p53 and epidermal growth factor receptor mRNA expression. Thus, transient axonal glycoprotein-1 increased apoptosis-related gene expression in U251 cells without inducing apoptosis. Instead, transient axonal glycoprotein-1 promoted the proliferation of these glioma cells.
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