Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Jun 21;21(11):1423–1435. doi: 10.1093/neuonc/noz107

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2019. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

PMC Copyright notice

Fig. 4 — SHP099 specifically inhibits cell cycle pathways in glioma cells with PDGFRα activation. (A) Heatmap of RNA-Seq analysis of differentially expressed genes (2-fold change and false discovery rate < 0.05) in Ink4a/Arf^−/− mAsts with ectopic expression of PDGFRα and PDGF-A treated with 0, 5, or 10 μM SHP099 in duplicate samples. (B) Expression of JUN after SHP099 treatment using RNA-Seq (left) and qRT-PCR (right) assays. (C) Gene Ontology analysis indicated that genes downregulated by SHP099 were associated with cell cycle pathways. (D) GSEA of SHP099-inhibited pathways using ranked gene expression changes in Ink4a/Arf^−/− mAsts with ectopic expression of PDGFRα and PDGF-A treated with 5 or 10 μM SHP099 compared with a vehicle control (0 μM SHP099). NES, normalized enrichment score. (E and G) Representative images from flow cytometric analysis of the influence of SHP099 treatment on cell cycle in Ink4a/Arf^−/− mAsts with ectopic expression of PDGFRα and PDGF-A (E) or LN444 cells with ectopic expression of an EV or PDGF-A (G). (F and H) Percentage of cells in G0/G1 phase in (E) and (G), respectively. *P < 0.05, **P < 0.01, ***P < 0.001, by one-way ANOVA.

Fig. 4 — SHP099 specifically inhibits cell cycle pathways in glioma cells with PDGFRα activation. (A) Heatmap of RNA-Seq analysis of differentially expressed genes (2-fold change and false discovery rate < 0.05) in Ink4a/Arf^−/− mAsts with ectopic expression of PDGFRα and PDGF-A treated with 0, 5, or 10 μM SHP099 in duplicate samples. (B) Expression of JUN after SHP099 treatment using RNA-Seq (left) and qRT-PCR (right) assays. (C) Gene Ontology analysis indicated that genes downregulated by SHP099 were associated with cell cycle pathways. (D) GSEA of SHP099-inhibited pathways using ranked gene expression changes in Ink4a/Arf^−/− mAsts with ectopic expression of PDGFRα and PDGF-A treated with 5 or 10 μM SHP099 compared with a vehicle control (0 μM SHP099). NES, normalized enrichment score. (E and G) Representative images from flow cytometric analysis of the influence of SHP099 treatment on cell cycle in Ink4a/Arf^−/− mAsts with ectopic expression of PDGFRα and PDGF-A (E) or LN444 cells with ectopic expression of an EV or PDGF-A (G). (F and H) Percentage of cells in G0/G1 phase in (E) and (G), respectively. *P < 0.05, **P < 0.01, ***P < 0.001, by one-way ANOVA.