PURPOSE: To address the role of ubiquitin-conjugating enzyme, E2C/UbcH10, in astrocytic carcinogenesis. METHODS: Expression pattern of UbcH10 in U251 glioma cells was evaluated by immunohistochemistry and western blot. RNA interference was employed to downregulate UbcH10 expression in U251 cell line. The effect of UbcH10 silencing on cell proliferation was assessed by MTT assay and cell cycle analysis. Cell apoptosis was determined by flow cytometry, TUNEL staining and western blot. RESULTS: Levels of UbcH10 protein were significantly upregulated in U251 cells compared with normal brain tissues. Marked immunoreactivity for UbcH10 was demonstrated in the cytoplasm of U251 glioma cells, especially in the mitotic cells. The growth rate of U251 cells was significantly inhibited by depletion of UbcH10 by short interference RNA. Further, UbcH10 RNAi induced apoptosis through induction of Bax and p53, downregulation of Bcl-2 and G2/M arrest of the cell cycle. CONCLUSION: These data imply that knocking-down UbcH10 protein expression may represent a potential therapeutic option for glioma.
PURPOSE: To address the role of ubiquitin-conjugating enzyme, E2C/UbcH10, in astrocytic carcinogenesis. METHODS: Expression pattern of UbcH10 in U251 glioma cells was evaluated by immunohistochemistry and western blot. RNA interference was employed to downregulate UbcH10 expression in U251 cell line. The effect of UbcH10 silencing on cell proliferation was assessed by MTT assay and cell cycle analysis. Cell apoptosis was determined by flow cytometry, TUNEL staining and western blot. RESULTS: Levels of UbcH10 protein were significantly upregulated in U251 cells compared with normal brain tissues. Marked immunoreactivity for UbcH10 was demonstrated in the cytoplasm of U251 glioma cells, especially in the mitotic cells. The growth rate of U251 cells was significantly inhibited by depletion of UbcH10 by short interference RNA. Further, UbcH10 RNAi induced apoptosis through induction of Bax and p53, downregulation of Bcl-2 and G2/M arrest of the cell cycle. CONCLUSION: These data imply that knocking-down UbcH10 protein expression may represent a potential therapeutic option for glioma.
Authors: Paul Kleihues; David N Louis; Bernd W Scheithauer; Lucy B Rorke; Guido Reifenberger; Peter C Burger; Webster K Cavenee Journal: J Neuropathol Exp Neurol Date: 2002-03 Impact factor: 3.685
Authors: Richa Batra; Nathalie Harder; Sina Gogolin; Nicolle Diessl; Zita Soons; Christina Jäger-Schmidt; Christian Lawerenz; Roland Eils; Karl Rohr; Frank Westermann; Rainer König Journal: PLoS One Date: 2012-12-12 Impact factor: 3.240