Hu et al. Journal of Experimental & Clinical Cancer Research 2010, 29:154 http://www.jeccr.com/content/29/1/154 Page 7 of 8 Figure 5 Inhibition of GSK-3b decreased NF- B-mediated expression of the antiapoptotic molecule survivin in ALL cells. Cells from patients with ALL were treated with controls (NaCl/ DMSO) or GSK-3b inhibitors (LiCl/SB216763) for 48 h. (A) The cell pellet was collected and RNA was obtained, then RT-PCR analysis was performed. (B) Survivin mRNA levels were normalized to GAPDH levels in each group. NaCl (48 ± 4)% vs. LiCl (5 mM (40 ± 5)%, 10 mM (36 ± 3)%); DMSO (44 ± 5)% vs. SB216763 (5 μM (38 ± 4)%, 10 μM (23 ± 3)%). (C) Total cell lysates were separated by SDS-PAGE, transferred to PVDF membrane, and immunoblotted with the indicated antibodies. *P < 0.05 vs. controls, **P < 0.01 vs. controls. DNA marker; 1: NaCl; 2: DMSO; 3: LiCl, 5 mM; 4: LiCl, 10 mM; 5: SB216763, 5 μM; 6: SB216763,10 μM. results provide evidence of GSK-3b as a novel potential therapeutic target in the treatment of ALL. Survivin, which is known to be regulated by NF- B [23], plays a major role in the suppression of apoptosis [24]. Our previous experiments have shown that the expression of the antiapoptotic gene survivin signifi- cantly increased in children with newly diagnosed acute leukemia (data not shown). Using malignant cells obtained from children with ALL, we have analyzed the effect of GSK-3b inhibition on NF- B-dependent gene expression involved in the survival of ALL cells. We found that both SB216763 and LiCl could inhibit the expression of survivin, thereby promoting cell apoptosis. Conclusions Our data demonstrated for the first time the involvement of GSK-3b in pediatric ALL cells, and not in adult leuke- mia cells, although GSK-3b inhibition played a similar role in inducing apoptosis in leukemia cells via in vitro activation of NF- B. Thus, inhibition of GSK-3b and of its target NF- B signaling pathway could represent a new promising approach for pediatric ALL therapy. Acknowledgements We thank doctors for providing technical assistance and insightful discussions during the preparation of the manuscript. Author details 1Laboratory of Oncology, Affiliated Children’s Hospital, Chongqing Medical University, No.136, Zhongshan 2nd Road, Yuzhong District, Chongqing 86 400014, China. 2Department of Hematology, Affiliated Children’s Hospital, Chongqing Medical University, No.136, Zhongshan 2nd Road, Yuzhong District, Chongqing 86 400014, China. Authors’ contributions YH collected the clinical data and samples, drafted and revised the article critically for important intellectual content. YX directed the conception and design of the study. QL participated in the design of the study. XG and RL assisted in acquisition, analysis and interpretation of data. All authors have seen and approved the final manuscript. Competing interests The authors declare that they have no competing interests. Received: 3 October 2010 Accepted: 26 November 2010 Published: 26 November 2010 References 1. Pui CH, Evans WE: Treatment of acute lymphoblastic leukemia. N Engl J Med 2006, 354:166-178. 2. Pui CH, Jeha S: New therapeutic strategies for the treatment of acute lymphoblastic leukaemia. Nat Rev Drug Discov 2007, 6:149-165. 3. Kaidanovich O, Eldar-Finkelman H: The role of glycogen synthase kinase-3 in insulin resistance and type 2 diabetes. Expert Opin Ther Targets 2002, 6:555-561. 4. 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