Leptin-induced Notch and IL-1 signaling crosstalk in endometrial adenocarcinoma is associated with invasiveness and chemoresistance

Figure 5 Inhibition of IL-1 R tI abrogates leptin induction of Notch in endometrial cancer cells. A, B: Representative results from Western Blot (WB) analysis of the effects of IL-1R tI antibodies on leptin-induced levels of Notch proteins (receptors: Notch1, Notch2, Notch3 and Notch4, and ligands: JAG1 and DLL4) in Ishikawa [A, type I endometrial cancer (EmCa)] and An3Ca cells (B, type II EmCa). Cells were cultured for 24h with leptin (0 and 1.2nM), leptin signaling inhibitor IONP-LPrA2 (IONP), and IL-1R tI antibodies (IL-1R tI Ab). Quantitative WB data (relative protein expression %) were calculated from densitometric analysis of bands with the NIH image program. The values were normalized to GAPDH as protein loading control. Data (mean ± SE) are representative of the results derived from a minimum of three independent experiments. ⁱP < 0.05 and ^jP < 0.01 vs basal (no leptin).