Nanoparticle-linked antagonist for leptin signaling inhibition in breast cancer

Figure 2 Ob-R expression and effect of IONP-LPrA2 on leptin-induced pSTAT3 and cyclin D1 levels in human breast cancer cells. A: Detection of Ob-R expression. The expression of Ob-R was detected by Western blot in MDA-MB-231, HCC1806, and MCF-7 cells; B: IONP-LPrA2 inhibition of leptin-induced pSTAT3 and cyclin D1 levels. Lysates were obtained from MDA-MB-231, HCC1806, and MCF-7 cells treated with leptin (1.2 nmol/L) or IONP-LPrA2 (0.0036 pmol/L) plus leptin (1.2 nmol/L) for 24-48 h. pSTAT3 and cyclin D1 levels were detected by Western blot. STAT3 served as a loading control for pSTAT3. GAPDH served as a loading control for cyclin D1; C: Densitometric analysis of pSTAT3 and cyclin D1 levels. Graphs represent quantitative analysis of pSTAT3 and cyclin D1 levels in MDA-MB-231, HCC1806, and MCF-7 cells with Image J software. Relative protein level was significantly increased in leptin treated cell lines compared to basal (untreated) cells, ^aP < 0.05. Relative protein level in cells pretreated with IONP-LPrA2 and then leptin differed significantly from those treated with leptin alone, ^cP < 0.05.