Etoposide

Staurosporine (STS), an apoptosis inducer, and U0126, an inhibitor of MEK, were purchased from Enzo Life Sciences, Inc. (Farmingdale, NY, USA). Etoposide (ETO), an apoptosis inducer, was purchased from Tokyo Chemical Industry Co., LTD. (Tokyo, Japan).
The following antibodies were used for western blot, immunoprecipitation, and immunofluorescence (IF) analysis: anti-N-cadherin (BD Transduction Laboratories, Franklin Lakes, NJ, USA), anti-Flag (Sigma Aldrich, MO, USA), anti-DR-5, anti-DcR-2, anti-Fas, anti-TNFR-1, and anti-TNFR-2 (Cell Signaling Technology, Inc., Danvers, MA, USA), anti-phospho extracellular signal-regulated kinase (ERK)1/2, anti-ERK1/2 (Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA), anti-phospho p38, anti-p38, anti-phospho Akt, anti-Akt, anti-phospho NF-kB p65, anti-NF-kB p65, anti-cleavage PARP (Cell Signaling Technology, Inc.), and anti-β actin (Sigma-Aldrich Corporation, St. Louis, MO, USA).
HOC313 and HOC719NE cells were transfected with N-cadherin small interfering RNA (si-CDH2) (Ambion, Life Technologies, Foster City, CA, USA) using Oligofectamine reagent (Invitrogen Corporation) following the manufacturer’s instructions.

HeLa cells purchased from Korean Cell Line Bank (KCLB; Seoul, Korea) were maintained in Dulbecco’s modified Eagle’s medium (Welgene, Daegu, Korea) supplemented with 10% heat inactivated fetal bovine serum (GIBCO, Grand Island, NY, USA) and 1% streptomycin and penicillin (GIBCO) at 37 °C and 5% CO₂ in humidified air. For the treatment of actinomycin D, HeLa cells were treated with dimethyl sulfoxide (DMSO, vehicle alone; Sigma-Aldrich, St. Louis, MO, USA) or 100 μM of etoposide (Tokyo Chemical Industry, Tokyo, Japan); 24 h later the medium was replaced with fresh, and actinomycin D was added at 5 μg/mL for the indicated times.