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. 2020 Sep;1865(9):158737. doi: 10.1016/j.bbalip.2020.158737

Fig. 5.

Fig. 5

TG catabolism and proliferation of Control/ATGL-OE cancer cells. (A, B) Proliferation of Control/ATGL-OE (A) B16 and (B) CT26 cells was analyzed with a hemocytometer at the indicated timepoints. (C) TG hydrolase activity of Control/ATGL-OE cancer cells and white adipose tissue (WAT) in the presence and absence of 50 ng/ml CGI-58 and 40 μM Atglistatin© (AI) was determined using cell/tissue lysates and a radiolabeled TG substrate. (D) TG content of Control/ATGL-OE cancer cells was determined after Folch extraction using a commercially available kit. (E) FA content of Control/ATGL-OE cancer cells was determined after Folch extraction using a commercially available kit. Data are presented as mean values of n = 3–6 ± standard deviation. Significance was determined by student's t-test (*p ≤ 0.05, **p ≤ 0.01 versus control group, #p ≤ 0.05, ##p ≤ 0.01 versus ATGL-OE group; $p ≤ 0.05, $$p ≤ 0.01 versus ATGL-OE + CGI-58 group).