Fig. 3: PGK1 induces cell proliferation via PRAS40 phosphorylation. | Cell Death & Disease

Fig. 3: PGK1 induces cell proliferation via PRAS40 phosphorylation.

From: PGK1 represses autophagy-mediated cell death to promote the proliferation of liver cancer cells by phosphorylating PRAS40

Fig. 3

A, B Cell counting for the indicated cells. The cells were treated with peptide control or peptide 241–256 (10 μM) (A). The cells depleted with PGK1 were introduced with empty vector, shRNA-resistant FLAG-PGK1, or FLAG-PGK1 T378P expression vector (B). C, D Cell counting and western blotting for the PGK1-depleted cells reintroduced with control, shRNA-resistant FLAG-PGK1 expression vector, or PRAS40 shRNA together with shRNA-resistant FLAG-PGK1 expression vector. E, F Cell counting and western blotting for the cells introduced with control, PGK1 shRNA (shPGK1), PGK1 shRNA together with Myc-PRAS40-expression vector, or PGK1 shRNA together with Myc-PRAS40 T246A expression vector. G–J HepG2 cells introduced with control, PGK1 shRNA, or PGK1 shRNA together with FLAG-PRAS40-expression vector, were injected into nude mice (n = 4). Tumor volumes were recorded every 2 days (G). On day 16, tumors were dissected and acquired. Images were taken (H), tumors were weighed (I), and the tumor tissue lysates were applied to western blotting (J). K, L HepG2 cells introduced with control, PGK1 shRNA, PGK1 shRNA together with Myc-PRAS40-expression vector, or PGK1 shRNA together with Myc-PRAS40 T246A expression vector were injected into nude mice (n = 6). On day 21, tumors were dissected and acquired. Images were taken (K), and tumors were weighed (L). Scale bar, 10 mm. Data represent the mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001. The quantification results of the band density were labeled above the bands.

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