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Downregulation of Phosphoserine aminotransferase 1 promotes tumorigenesis in Glioblastoma
Author(s) -
Chan Yung-chieh,
Huang Shang-Pen,
Chang Yu-Chan,
Hsiao Michael
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.04967
Subject(s) - downregulation and upregulation , carcinogenesis , gene knockdown , cancer research , u87 , western blot , cell growth , microarray analysis techniques , biology , cell culture , chemistry , medicine , glioblastoma , cancer , gene , gene expression , genetics
Glioblastoma (GBM) is a typical brain tumor with survival below ten percent at 5 years after diagnosis. The genetic alternation and histological features are integrated into the classification of gliomas for better clinical management of GBM. However, the development of therapeutic strategies and diagnosis for GBM patients remains poor. In this study, we found that downregulation of phosphoserine aminotransferase ( PSAT1 ) mediated tumorigenesis of GBM. Analyses of available clinical datasets showed that PSAT1 downregulation was associated with poor survival of GBM patients. In western‐blot analysis of our GBM cell panel, PSAT1 protein was shown to be overexpressed in U87 and SNB75 cells, but downregulated in T98G and G9t cells. We overexpressed PSAT1 in T98G and G9T cells and knocked down PSAT1 in U87 and SNB75 cells for further study. The colony formation assay showed that PSAT1 overexpression inhibited clonal expansion in T98G and G9T cells. PSAT1 knockdown promoted cell growth in U87 and SNB75 cells. Furthermore, PSAT1 knocked‐down cells revealed significant tumorigenesis in mouse xenograft tumor model. The microarray assay indicated that downregulation of PSAT1 plays an important role in GBM tumorigenesis.