Abstract
Activation of AMPK inhibits medulloblastoma cell growth and Gli1 activity
Highlights
The sonic hedgehog (SHH) pathway is a highly-conserved pathway important for cellular growth and differentiation [1,2]
High Gli1 expression was not detected in the inner external granule layer (EGL) and internal granule layer (IGL) cells stained with NeuN, a marker for differentiating granule cells (GCs)
NIH3T3 cells and mouse embryonic fibroblast (MEF) cells were regularly passaged in DMEM supplemented with 10% bovine calf serum (BCS) and DMEM supplemented with 10% fetal bovine serum (FBS), respectively
Summary
The sonic hedgehog (SHH) pathway is a highly-conserved pathway important for cellular growth and differentiation [1,2]. Modifications of SHH signaling loci in transgenic mice in Corrales et al 2004 demonstrated that the spatial and temporal coordination of SHH signaling and Gli expression regulates both cellular and anatomical development of the cerebellum. A recent finding in Scientific Reports suggested a role for metabolic sensor AMP-activated kinase (AMPK) with SHH signaling-mediated cerebellar development. Mice harboring conditional knockouts of LKB1, mediated through Atoh1-Cre expression confined to the cerebellar granule cell precursors (in addition to the inner ear, spinal cord, and intestines), were found to exhibit abnormal foliation concurrent with increased SHH target gene expression [13]. We review evidence that AMPK regulates murine Gli, providing the critical groundwork for mouse models of AMPK regulation of SHH signaling in cerebellar development and preclinical studies employing AMPK activation
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