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Fig. 1 | BMC Cancer

Fig. 1

From: β-arrestin1-mediated acetylation of Gli1 regulates Hedgehog/Gli signaling and modulates self-renewal of SHH medulloblastoma cancer stem cells

Fig. 1

Low levels of miR-326 characterize SHH-MB CSCs. a Left: Western blot (WB) analysis of endogenous Hh/Gli and stemness markers levels in pre-oncosphere cell population (T0) and oncospheres (CSCs) derived Ptch1+/− mice model of SHH-MB. Loading control (LC): Actin. Right: Immunofluorescence of nuclear Hoechst (blue) staining with Nanog or Nestin (green) in CSCs. Scale bar: 10 ⌠m. b miR-326 expression levels in MB cells grown in SM (CSCs) vs pre-oncosphere cell population (T0) are expressed in arbitrary units (AU). Bar graphs represent mean ± S.D. from three independent experiments. *p < 0.05. c Left panel: WB analysis of endogenous Hh/Gli, stemness and differentiation markers levels in CSCs grown as oncospheres in SM and exposed to differentiation stimuli (DFM). LC: Actin. Right panel: Immunofluorescence of nuclear Hoechst (blue) staining with Nanog or Gli1 (green) in CSCs grown in SM or DFM. Scale bar: 10 μm. d miR-326 expression levels in MB cells grown in SM (CSCs) or in DFM

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BMC Cancer

ISSN: 1471-2407

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