Fig. 6

Leptin promotes CCN5 expression via activation of JAK/STAT3/Akt signaling mechanism. a MCF-7 and ZR-75-1 cells were serum deprived for 24 h and then grown again in serum-deprived MDEM in the presence or absence of leptin (3.215 nM) for 48 h and the status of phosphorylation of STAT3, p-AKT and p-ERK1/2 and constitutive expressions of these three proteins were measured using Western blot analysis. β-actin was used as loading controls. Error bars indicate mean ± SEM of three independent experiments. b Semi-confluent (~ 60–70%) MCF-7 and ZR-75-1 cells were grown in serum-deprived MDEM for 24 h, and then treated with different pharmacological inhibitors [AG-490 (100 μM), Wortmannin (20 μM) and U0126 (10 μM)] for 1 h. Following treatments of inhibitors, cells were grown in the presence or absence of leptin for 48 h. CCN5 levels were measured in the cell extracts using Western blot analysis. The doses of the inhibitors are obtained from the vendors’ instruction manuals. Error bars indicate mean ± SEM of three independent experiments. NS, non-significant, *p < 0.0001vs control. c Effects of different inhibitors on CCN5 expression and activities of p-STAT3 and p-AKT in MCF-7 cells. Error bars indicate mean ± SEM of three independent experiments. JAK2-i, JAK2-inhibitor and AKT-i, AKT-inhibitor