“…20 Nishikawa et al demonstrated that ASCL1 directly activates miR-375, which functions as a sufficient inducer of neuroendocrine differentiation. 14 Repressor MYBPH TGF-β-mediated epithelial-to-mesenchymal transition 36,37 POU-III/IV POU Activator POU-III/IV, ASCL1, NeuroD1, TTF1, neuroendocrine markers (NCAM1, SYP, CGA) Organigenesis of brain and nervous systems Unknown 35,[38][39][40][41][42][43] POU-III/IV: class III/IV POU; bHLH, basic helix-loop-helix; SYP, synaptophysin; ALDH1A1 aldehyde dehydrogenase 1A1; CIITA, class II transactivator; DKK1, Dikkopf WNT signaling pathway inhibitor 1; CDH1, cadherin 1 (E-cadherin); NCAM1, neural cell adhesion molecule 1; IGFBP2, insulin-like growth factor binding protein 2; CGA, chromogranin A; MYBPH, myosin binding protein H. ASCL1 was also reported to upregulate synaptophysin and increase tumor-initiating capacity via upregulation of the candidate stem cell markers CD133 and aldehyde dehydrogenase 1A1 (ALDH1A1). 15,16 Neuronal differentiation 1 (NeuroD1) NeuroD1 (also known as BETA2, BHF-1, MODY6, NeuroD, or bHLHa3) is also a member of the basic helix-loop-helix family of transcription factors and plays crucial roles in the development of pancreatic islets and the cerebellum, hippocampus, inner ear sensory ganglia, and retinal photoreceptor cells.…”