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. 2020 Dec 4;7:608441. doi: 10.3389/fmed.2020.608441

Figure 4.

Figure 4

miR-206/FAM83A/PI3K/AKT signaling pathway molecules serve as critical effectors in cervical cancer progression. (A) GSEA plot showing that FAM83A expression was correlated with PI3K/AKT signaling-related gene signatures. (B) Protein levels of PI3K, p-PI3K, AKT, p-AKT, mTOR, and p-mTOR in CaSki cells are shown, and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as a loading control. (C) Schematic of binding sites in the FAM83A 3'-UTR complementary to the “seed region” of miR-206. Correlation analysis of FAM83A expression and miR-206. (D) The overexpression of miR-206 dramatically decreased the protein expression of FAM83A in CaSki cells. (E) The complementary sequences or the mutant (underlined) binding site of FAM83A or the miR-206 binding site in the 3'-UTR of FAM83A from different mammalian species. (F) Summary of the mechanism of FAM83A in cervical cancer. Error bars represent the means of three independent experiments. *P < 0.05, **P < 0.01.