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. 2021 Mar 26;12(4):328. doi: 10.1038/s41419-021-03596-w

Fig. 7. Src/PI3K/AKT is a key pathway by which CD36 activates mTOR.

Fig. 7

A Western blot analysis of Src, p-Src (tyr416), AKT, p-AKT (Ser43), PI3K, and p-PI3K expression both in SK-Hep-1 and Huh7 cells (n = 3). The relative quantification of the target proteins was shown on the right. B SK-Hep-1 and Huh7 cells were pretreated with BKM-120 (BKM, 1 μM) before analyzing mTOR signaling pathway (n = 3). The ratio of p-mTOR/mTOR was shown on the right. C Proliferation of HCC cells treated with or without BKM-120 (1 μM), an inhibitor of PI3K (n = 6). Wound-healing (D) and transwell assays (E) were used to evaluate the migration of HCC cells with or without BKM (n = 10). F Proliferation of HCC cells treated with or without MK-2206 (MK, 5 μM), an inhibitor of AKT (n = 6). Wound-healing (G) and transwell assays (H) were used to evaluate the migration of HCC cells with or without MK (n = 10). All data are presented as mean ± SD. *P < 0.05, **p < 0.01, and ***p < 0.001 compared with the NC group, #P < 0.05, ##P < 0.01, and ###p < 0.001 compared with the group without BKM or MK. P-value was calculated using Student’s t-test (A) and one-way analysis of variance with Tukey’s multiple comparison tests (B–H).