PTPRN promotes glioma cell proliferation, migration, and invasion by regulating the EMT pathway

PTPRN通过调控EMT通路促进胶质瘤细胞增殖、迁移和侵袭。

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Abstract

Glioma is a highly aggressive malignancy with no effective treatment. This study investigates the role of protein tyrosine phosphatase receptor type N (PTPRN) in glioma progression. The U87 human glioma cell line was used to monitor proliferation, invasion, and migration during PTPRN knockdown. The viability, migration, and invasion were analyzed using the Cell Counting Kit-8 assay, transwell migration, and invasion assays. Additionally, the expression of proteins associated with the cell cycle was examined using western blotting. The knockdown of PTPRN resulted in a reduction in glioma cell proliferation, migration, and invasion, as well as the expression of cell cycle markers like cadherin 1 (CDH1), matrix metalloproteinase 9 (MMP9), snail family transcriptional repressor 1 (SNAI1), and others. Among these genes, MMP9 and SNAI1 are core genes that link PTPRN and the epithelial-mesenchymal transition (EMT) pathway. PTPRN, a key molecule associated with the EMT pathway, can be used as a molecular marker for tumor risk assessment, detection, and diagnosis in the early stages of glioma.

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