Fig. 3

Specific knockdown of ErbB3 expression or blocking of its downstream signaling potentiates VPA-induced apoptosis in pancreatic cancer cells. a HPAF-II and MPanc96 cells were infected with ConshRNA- or ErbB3shRNA-expressing letiviruses. After 24 h, infected cells were subjected to selection with puromycin (1 μg/mL) for additional 24 h. Cells were then harvested and subjected to western blot analyses with specific antibodies directed against ErbB3, P-Akt, Akt, P-MAPK, MAPK or β-actin. b Growth curves of HPAF-II and MPanc96 cells without or with specific knockdown of ErbB3 expression. c, d HPAF-II and MPanc96 cells without or with transient knockdown of ErbB3 expression were cultured with RPMI1640 (0.5% FBS) in the presence or absence of VPA (0.5 mmol/L) for 24 h. Cells were harvested and subjected to antibodies directed against PARP, Cleaved-Caspase-3 or β-actin (c), or apoptotic ELISA (d). e, f HPAF-II and MPanc96 cells untreated or treated with either VPA (0.5 mmol/L) or LY294002 (10 μmol/L) alone, or combinations of VPA and LY294002 for 24 h were collected and subjected to western blot analyses with specific antibodies directed against PARP, C-Casp-3 or β-actin (e) or apoptotic-ELISA (f). Bars, S.D. Data show the representative of three independent experiments