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. 2021 Mar 12;11(11):5387–5403. doi: 10.7150/thno.42345

Figure 6.

Figure 6

The AKT pathway is involved in PRMT1-regulated LCN2 expression in ccRCC cells. (A) The AKT pathway was inactivated after PRMT1 knockdown in Caki-1 cells, but no effect on the ERK1/2 and NF-κB pathways was observed. (B) DCPT1061 inhibited AKT and RB phosphorylation in Caki-1 cells. (C) Knockdown of LCN2 inhibited AKT and RB phosphorylation in Caki-1 cells. (D) Exogenous LCN2 stimulation at different concentrations induced AKT-RB activation in Caki-1 and A498 cells. (E) Exogenous LCN2 stimulation (200 ng/ml) reactivated the AKT-RB pathway in DCPT1061 treated Caki-1 cells. (F) The AKT-RB pathway was inactivated after NGALR siRNAs knockdown in Caki-1 and A498 cells, as compared with the scrambled control. (G) Exogenous LCN2 stimulation (200 ng/mL) barely activated the AKT-RB pathway in NGALR-deleted Caki-1 cells.