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Fig. 4 | Molecular Cancer

Fig. 4

From: Role of MEK partner-1 in cancer stemness through MEK/ERK pathway in cancerous neural stem cells, expressing EGFRviii

Fig. 4

High expression of LAMTOR3 in F3.EGFRviii spheres is associated with ERK1/2 activation. a The levels of pAKT, pMEK1/2, and pERK1/2 in adherent and spheroid F3.EGFRviii cells were determined by immunoblot analysis, using α-tubulin as a loading control. b Expression profile analysis of a MAPK signaling-associated gene set through MAPK pathway superarray in F3.EGFRviii cells and F3.EGFRviii spheres (red, genes upregulated >2-fold; blue, genes downregulated >2-fold; gray, no significant change). The black arrow indicates LAMTOR3. c GEO analysis to deduce candidate genes that distinguish signaling in F3.EGFRviii spheres. Three independent GSE studies, two using primary brain tumor cells (GSE23806, GSE15824) and one using induced cancer stem cells from neuroblastoma samples (GSE44537), were used to select commonly altered genes. Candidate genes were narrowed down using gene ontology for ‘protein complex scaffold’ genes. Red and blue indicate upregulated or downregulated genes, respectively. d The expression of LAMTOR3 in adherent F3.EGFRviii cells and F3.EGFRviii spheres was determined by real-time PCR (n = 3). e The levels of MP1, SIRT1, and pERK1/2 were determined by immunoblotting in adherent and spheroid F3.EGFRviii cells using α-tubulin as a loading control

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