PURPOSE: Treatment for high-risk neuroblastoma is still challenging. The purpose of the present study was to determine whether thalidomide suppresses etoposide-induced NF-κB activation and thus potentiates apoptosis in murine neuroblastoma. METHODS: A murine neuroblastoma cell line, C1300, and A/J mice were used in this study. We evaluated NF-κB activation after using etoposide with or without thalidomide by quantitative analysis of NF-κB by ELISA and by Western blot analysis of IκB phosphorylation in vitro and in vivo. Induction of apoptosis was evaluated by Western blot analysis of the apoptotic signals caspase-3, 8, and 9 in vitro and by TUNEL assays in vivo. We also evaluated the efficacy of the combination of etoposide and thalidomide by assessing tumor growth and mouse survival in vivo. RESULTS: Etoposide activated NF-κB in C1300 cells. This activation was suppressed by thalidomide and IκB was re-upregulated. The apoptotic signals were enhanced by the combination of thalidomide and etoposide compared with etoposide alone in vitro, which was consistent with TUNEL assays. The combination of etoposide and thalidomide also slowed tumor growth and mouse survival. CONCLUSION: Thalidomide potentiates etoposide-induced apoptosis in murine neuroblastoma by suppressing NF-κB.
PURPOSE: Treatment for high-risk neuroblastoma is still challenging. The purpose of the present study was to determine whether thalidomide suppresses etoposide-induced NF-κB activation and thus potentiates apoptosis in murineneuroblastoma. METHODS: A murineneuroblastoma cell line, C1300, and A/J mice were used in this study. We evaluated NF-κB activation after using etoposide with or without thalidomide by quantitative analysis of NF-κB by ELISA and by Western blot analysis of IκB phosphorylation in vitro and in vivo. Induction of apoptosis was evaluated by Western blot analysis of the apoptotic signals caspase-3, 8, and 9 in vitro and by TUNEL assays in vivo. We also evaluated the efficacy of the combination of etoposide and thalidomide by assessing tumor growth and mouse survival in vivo. RESULTS:Etoposide activated NF-κB in C1300 cells. This activation was suppressed by thalidomide and IκB was re-upregulated. The apoptotic signals were enhanced by the combination of thalidomide and etoposide compared with etoposide alone in vitro, which was consistent with TUNEL assays. The combination of etoposide and thalidomide also slowed tumor growth and mouse survival. CONCLUSION:Thalidomide potentiates etoposide-induced apoptosis in murineneuroblastoma by suppressing NF-κB.
Authors: Cristina Maria de Souza; Ana Cândida Araújo e Silva; Clarissa de Jesus Ferraciolli; Giovanna Vieira Moreira; Liliane Cunha Campos; Diego Carlos dos Reis; Miriam Teresa Paz Lopes; Mônica Alves Neves Diniz Ferreira; Silvia Passos Andrade; Geovanni Dantas Cassali Journal: Biomed Pharmacother Date: 2013-08-26 Impact factor: 6.529
Authors: Murali Chintagumpala; Susan M Blaney; Lisa R Bomgaars; Aleksander Aleksic; John F Kuttesch; Renee A Klenke; Stacey L Berg Journal: J Clin Oncol Date: 2004-11-01 Impact factor: 44.544
Authors: Roberto Ciaccio; Piergiuseppe De Rosa; Sara Aloisi; Marta Viggiano; Leonardo Cimadom; Suleman Khan Zadran; Giovanni Perini; Giorgio Milazzo Journal: Int J Mol Sci Date: 2021-11-28 Impact factor: 5.923