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. Author manuscript; available in PMC: 2011 May 30.
Published in final edited form as: Biochem Pharmacol. 2009 Jun 18;78(9):1105–1114. doi: 10.1016/j.bcp.2009.06.009

Fig. 7.

Fig. 7

Schematic presentation of the molecular components and pathways to show induction of differentiation and apoptosis in neuroblastoma cells. Treatment of cells with 4-HPR induced differentiation with upregulation of the tight junction protein e-cadherin and down regulation of Notch-1, Id2, and fibronectin. Combination of 4-HPR and GST reactivated the expression of tumor suppressors (p53, p21, Rb and PTEN), which inhibited the N-Myc mediated mitogenic/oncogenic signals leading to suppression of cellular proliferation as evidenced by down regulation of hTERT and PCNA. Pretreatment of cells with 4-HPR potentiated GST mediated cell cycle arrest and induction of both extrinsic and intrinsic pathways of apoptosis in neuroblastoma cells.