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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Inhibition of choline metabolism in an angioimmunoblastic T-cell lymphoma preclinical model reveals a new metabolic vulnerability as possible target for treatment

Fig. 2

mAITL plck-GAPDH tumor cells rely on the CDP-choline pathway for increased phosphatidylcholine production. CD4 + PD-1high cells were isolated from pLck-GAPDH mouse lymphoma and compared to WT CD4 + splenocytes for proteomic data analysis. Principle component analysis for the two groups in is shown in (A) and data are represented by a volcano plot in (B). C Expression data for the enzymes implicated in the CDP-ethanolamine pathway, Etnk1and Pcyt2 (blue quadrants) and the levels of phosphatidylethanolamine lipids (PE, black quadrants), the resulting end product of this pathway are shown for murine CD4 + PD-1high cells tumor cells (GAPDH +) versus WT CD4 + splenocytes (D) Expression data for the three enzymes implicated in this CDP-choline pathway ChK, Pcyt1A, CEPTt1 (in green quadrant) and the levels of produced lipids in this pathway (phosphocholine and phosphatidylcholine (PC)) are shown in the red quadrants for murine CD4 + PD-1high cells tumor cells (GAPDH +) versus WT CD4 + splenocytes. E Differences in expression levels of LPCAT the enzyme converting lysophosphatidylcholine (LPC) into PC is shown for both conditions in a blue quadrant. LPC levels are indicated in (E) Sphingomyelin levels (SM) are indicated for both conditions in (F). Data are represented as mean ± SD (Box and whisker plot representation, WT n = 5, GAPDH n = 8, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns Not significant)

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