Fig 2: CaMKK2 downregulation suppressed PI3K, PDK1 and Akt mRNA levels in OV90 cells. (A-D) RT-qPCR analysis was used to detect the mRNA expression of CaMKK2 (A), PI3K (B), PDK1 (C) and Akt (D) in OV90 cells. *P <0.05.

Fig 3: CaMKK2 downregulation suppressed PI3K, PDK1 and Akt protein levels in OV90 cells. (A-D) Western blot was performed to determine the protein expression of CaMKK2, PI3K, PDK1 and Akt in OV90 cells. (E) The representative images from western blot results in OV90 cells before transfection. (F) The representative images from western blot results in OV90 cells after transfection. *P <0.05.

Fig 4: PDK1 was a direct target of miR-4290 in HEK-293 cells. A, The putative binding sites between miR-4290 and PDK1 and the mutated binding sites. WT, wide type; MUT, mutated type. B, The luciferase gene reporter assay was used to evaluate the relationship between miR-4290 and PDK1 after cell transfection with Negative Control (NC) mimics or miR-4290 mimics (n=3, **P<0.01). C, Western blotting analysis on the protein expression level of PDK1 after HEK-293 cells were transfected with Control, miR-4290, NC inh, or miR-4290 inh, and D, PDK1 RNA level (n=3, **P<0.05, compared with Control; ##P<0.05, compared with NC inh group). Data are reported as means±SD (ANOVA).

Fig 5: miR-4290 suppressed the glycolysis of gastric cancer cells via targeting PDK1. A and B, RT-PCR and western blotting assays were used to detect the mRNA and protein expression levels of PDK1 after SGC7901 and HGC-27 cells were transfected with Vector or PDK1 (n=3, **P<0.01). C, The glycolysis indicators, including lactate, glucose uptake, and ATP production were examined after SGC7901 and HGC-27 cells were transfected with Control mimics+Vector, miR-4290 mimics+Vector, and miR-4290 mimics+PDK1 (n=3, **P<0.01, compared with Control mimics+Vector group; ##P<0.01, compared with miR-4290 mimics+Vector group). Data are reported as means±SD (ANOVA or t-test).