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. Author manuscript; available in PMC: 2021 Oct 15.
Published in final edited form as: Cancer Res. 2021 Feb 16;81(8):2086–2100. doi: 10.1158/0008-5472.CAN-20-2218

Figure 5. Ritanserin induces phospholipid reprogramming in Tsc2-deficient cells.

Figure 5.

(A) Schematic representation of diacylglycerol metabolism to phosphatidic acid via DGKA. (B) Phosphatidic acid levels are elevated in Tsc2−/− MEFs compared to Tsc2+/+ MEFs. Ritanserin treatment (10uM; 16 hours) decreases PA levels in Tsc2−/− MEFs but not in Tsc2+/+ MEFs. (C-G) DGKA inhibition by ritanserin leads to accumulation of diacylglycerol and phospholipids PI, PC, PS and PE similarly in Tsc2−/− MEFs and in Tsc2+/+ MEFs. Data presented as mean ± SD of the sum of each lipid species from three biological replicates. Statistical significance was assessed using t-test with FDR correction (q<0.05) and *p<0.05, **p<0.01, ***p<0.001, ****p <0.0001.