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Expression of TAG1/APP signaling pathway in the proliferation and differentiation of glioma stem cells.

ABSTRACT: The aim of the present study was to examine the role of the expression of transient axonal glycoprotein-1 (TAG1)/precursor protein (APP) signaling pathway in the proliferation and differentiation of glioma stem cells. A glioma cell line (U373) was used as well as fluorescence quantitative PCR, western blot analysis, and enzyme-linked immunosorbent assay (ELISA), to examine the role of the expression of TAG1/APP signaling pathway in the proliferation and differentiation of glioma stem cells after five generations of in vitro culture. The results showed that compared to the normal glioma cells, the expression of TAG1 and APP was significantly increased in the proliferation of glioma stem cells. The results of ELISA and western blot analysis also confirmed a significant elevation in the protein expression of TAG1 in glioma stem cells compared to normal human glioma cells. When glioma stem cells were cultured in differentiation medium, as revealed by RT-PCR, the expression of TAG1 and APP in glioma stem cells initially increased and then decreased. In addition, the protein expression of TAG1 and APP was consistent with the RT-PCR results. Compared with undifferentiated glioma stem cells, the expression of TAG1 and APP decreased gradually with the extension of differentiation time. In conclusion, the expression of TAG1/APP signaling pathway in glioma cells was abnormal. Thus, this pathway is involved in the proliferation and differentiation of glioma cells and promotes the proliferation of glioma cells to inhibit the differentiation of glioma cells.

SUBMITTER: Zhen YB

PROVIDER: S-EPMC5530010 | biostudies-other | 2017 Aug

REPOSITORIES: biostudies-other

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Project description:Tumor heterogeneity of high-grade glioma (HGG) is recognized by four clinically relevant subtypes based on core gene signatures. However, molecular signaling in glioma stem cells (GSCs) in individual HGG subtypes is poorly characterized. Previously we identified and characterized two mutually exclusive GSC subtypes with distinct activated signaling pathways and biological phenotypes. One GSC subtype presented with a gene signature resembling Proneural (PN) HGG, whereas the other was similar to Mesenchymal (Mes) HGG. Classical HGG-derived GSCs were sub-classified as either one of these two subtypes. Differential mRNA expression analysis of PN and Mes GSCs identified 5,796 differentially expressed genes, revealing a pronounced correlation with the corresponding PN or Mes HGGs. Mes GSCs displayed more aggressive phenotypes in vitro and as intracranial xenografts in mice. Further, Mes GSCs were markedly resistant to radiation compared with PN GSCs. Expression of ALDH1A3 - one of the most up-regulated Mes representative genes and a universal cancer stem cell marker in non-brain cancers - was associated with self-renewal and a multi-potent stem cell population in Mes but not PN samples. Moreover, inhibition of ALDH1A3 attenuated the growth of Mes but not PN GSCs in vitro. Lastly, radiation treatment of PN GSCs up-regulated Mes-associated markers and down-regulated PN-associated markers, whereas inhibition of ALDH1A3 attenuated an irradiation-induced gain of Mes identity in PN GSCs in vitro. Taken together, our data suggest that two subtypes of GSCs, harboring distinct metabolic signaling pathways, represent intertumoral glioma heterogeneity and highlight previously unidentified roles of ALDH1A3-associated signaling that promotes aberrant proliferation of Mes HGGs and GSCs. Inhibition of ALDH1A3-mediated pathways therefore might provide a promising therapeutic approach for a subset of HGGs with the Mes signature. Here, we describe the gene expression analysis, including pre-processing methods for the data published by Mao and colleagues in PNAS [1], integration of microarray data from this study with The Cancer Genome Atlas (TCGA) glioblastoma data and also with another published study.

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Expression of TAG1/APP signaling pathway in the proliferation and differentiation of glioma stem cells.

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