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. Author manuscript; available in PMC: 2017 Jun 14.
Published in final edited form as: Cell Metab. 2016 May 19;23(6):1140–1153. doi: 10.1016/j.cmet.2016.04.016

Figure 6. Tumor growth is attenuated in HCT-116 cells lacking MTHFD2.

Figure 6

a. Western blot of folate metabolism genes in HCT-116 cells and two MTHFD2 deletion clones. b. Cell growth in complete media. c. Steady-state AICAR levels. d. dTTP labeling from [2,3,3-2H]serine (48 h). e. Fraction of malate redox-active hydrogen derived from serine as per figure 4b. f. 2H-labeling into palmitate from [2,3,3-2H]serine. Inset shows associated NADPH labeling fraction. g. Growth of HCT-116 cells in media without serine or glycine. h. Growth of HCT-116 mthfd2Δ_a cells require either serine or formate (1 mM). i. Growth of HCT-116 mthfd2Δ_a cells require either glycine of NAC (1 mM). j. Intratumor metabolite levels (AICAR and serine) from WT and deletion tumors implanted in CD-1 nude mice and measured by LC-MS (n=8–10). k. Tumor growth (volume ±SEM as measured by calipers) in nude mice containing subcutaneous tumors from HCT-116 WT and mthfd2Δ cells (n=10). l. Final tumor weights from tumor growth experiment in (k). * p<0.05; ** p<0.01; *** p<0.001 by unpaired t-test.