Figure 1.
DGAT Loss Reduces Tumor Growth and Alters Lipid Composition In Vivo
(A) Diagram of fatty acid and lipid synthesis and the influence of O2 and exogenous lipid.
(B) Growth curves for A498 xenograft tumors with induced (doxycycline chow) and un-induced (control chow) DGAT1 and DGAT2 shRNAs (hereafter called DGAT shRNA).
(C) Tumor weights after necropsy.
(D) Immunohistochemistry for cleaved caspase-3 and Ki67 in xenograft tumors collected on day 5 of treatment, with accompanying quantification.
(E) Total TG abundance derived from summing individual TG species abundance after liquid chromatography-mass spectrometry (LC-MS) quantification.
(F) TG species binned according to the number of fully saturated FA chains present and the abundance of each category summed and displayed as a ratio of doxycycline-treated versus control groups.
All results are means of n = 10 tumors (2 tumors per mouse) per arm; error bars represent ± SD (B, D, and F) or ± SEM (C). Statistical significance by t test or ANOVA, as appropriate; ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001. ACC, acetyl-CoA carboxylase; CE, cholesterol ester; DG, diglyceride; DGAT, diglyceride acyltransferase; FASN, fatty acid synthase; ns, non-significant; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PS, phosphatidylserine; SCD(i), stearoyl-CoA desaturase (inhibitor); SFA, saturated FA; TG, triglyceride; UFA, unsaturated FA. See also Figure S1.