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Fig. 1 | Cancer & Metabolism

Fig. 1

From: Metabolic convergence on lipogenesis in RAS, BCR-ABL, and MYC-driven lymphoid malignancies

Fig. 1

MYC regulates lipogenesis genes. A Eμ-MYC model of B cell lymphoma RNA-seq reveal upregulation of de novo fatty acid lipogenesis genes linked to MYC expression as the B cell lymphoma progresses (GSE 51011). B RNA-seq profiles of lipogenesis genes from Eμ-tTA/Tet-O-MYC model T-ALL. Data mining experiments of MYC on vs off state in the Eμ-tTA/Tet-O-MYC primary model of T-ALL, inclusive of the FVB/N background shows MYC-dependent regulation of lipogenesis genes in vivo. (GSE106078). C RNA-seq was performed on cell lines (4188) derived from Eμ-tTA/Tet-O-MYC transgenic model in a MYC-off time-course. Decreased expression values were observed for fatty acid synthesis pathway genes (GSE178580) after MYC expression is abrogated. D Oncogenic MYC is stabilized by S62 phosphorylation and PIN1 mediated isomerization (for review see Cohn et al. [30]). GSK3beta initiates MYC recycling and is inhibited by both RAS and BCR-ABL, leading to a potential convergence on MYC-mediated programs. MYC is known to activate transcription of GLS which facilitates the entry of glutamine into the Krebs cycle. E Graphical representation of the fatty acid synthesis pathway, and chemical inhibitors of the de novo fatty acid synthesis are shown (red). F Cells derived from conditional transgenic murine models with differing oncogenic drivers. Conditional expression of the initiating oncogene is controlled by a Tet-Off system. The suppression of MYC or BCR-ABL or RAS results in reduced mRNA expression of specific genes known to facilitate de novo lipogenesis pathway, indicating a common feature of lymphoid malignancies regardless of the initiating oncogene. Values were normalized to ubiquitin controls and reported as fold change relative to MYC on condition (vehicle). *P0.1; **P 0.01; **P 0.001; ***P 0.001; ****P 0.0001

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