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. 2022 Jan 6;12(6):2887–2904. doi: 10.1016/j.apsb.2021.12.023

Figure 2.

Figure 2

GPS inhibited the interaction between PAQR3 and P110α to promote the activation of the PI3K/AKT pathway in vitro. (A) LY294002 reversed the up-regulation of p-PI3K, p-AKT and p-GSK3β induced by GPS co-treatment in PA-treated HepG2 cells (n = 3). ∗∗∗P < 0.001, ∗∗P < 0.01 vs. control group; ###P < 0.001, ##P < 0.01 vs. insulin-induced group; ^P < 0.01 vs. PA + insulin-induced group; &&P < 0.01 vs. insulin + PA + GPS-treated group. (B) Palmitatic acid stimulation increased the protein expression of PAQR3 in the Golgi apparatus in a time-dependent manner (n = 3). ∗∗P < 0.01, ∗P < 0.05 vs. 0 h. (C) The expression of PAQR3 and p110α in the Golgi apparatus in GPS co-treated HepG2 cells (n = 3). ∗∗P < 0.01 vs. Control group; ##P < 0.01 vs. PA-induced group, ns: no significance. (D) A co-immunoprecipitation assay was performed to detect the combination of PAQR3 and p110α in vitro. (E) Immunofluorescence staining presented the distribution and co-localization of PAQR3 and P110α in HepG2 cells, scale bar = 20 μm. (F) A co-immunoprecipitation assay was performed to detect the combination of p110α and p85α in HepG2 cells. (G) The expression of PAQR3 and p110α in the Golgi apparatus of HepG2 cells (n = 3). ∗∗∗P < 0.001 vs. control group; ##P < 0.01 vs. PA-induced group; ^P < 0.001 vs. PA + GPS-treated group. (H) The interaction between P110α and P85α in PA-treated HepG2 cells. (I) PAQR3 overexpression reversed the up-regulation of p-PI3K and p-AKT in PA-induced HepG2 cells (n = 3). ∗∗P < 0.01 vs. control group; ##P < 0.01 vs. insulin-induced group; ^P < 0.01 vs. PA + insulin-induced group; &&P < 0.01 vs. PA + insulin + GPS treated group. Protein level was quantified and normalized to α-tubulin in the control group cells. The data are presented as mean ± SD, and all experiments were performed at least three times with similar results. ns, no significance.