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. 2015 Jun 24;4(9):1404–1416. doi: 10.1002/cam4.484

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© 2015 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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NOTCH1 transcriptional activity was regulated by RND3, and inhibition of Notch activity diminished RND3 deficiency-induced GBM cell proliferation. (A) Addition of RND3 inhibited luciferase activity driven by CSL-responsive elements (left panel); and knockdown of RND3 promoted the luciferase activity (right panel). (B) Quantitative chromatin immunoprecipitation (ChIP) assay showed that NICD transcription-binding activity was significantly diminished along with the increase in RND3 expression levels in the HES1 promoter region. (C) Forced expression of RND3 inhibited U251 cell growth and the addition of NICD abolished the inhibitory effect of RND3 on cell proliferation. (D) Knockdown of RND3 promoted cell growth and compound E (Comp E) treatment impeded RND3 deficiency-induced cell proliferation. (E) Knockdown of NOTCH1 by siRNA (siNotch1) also abolished RND3 deficiency-induced cell proliferation.