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• W2313385191 abstract "Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FLPancreatic endocrine tumors occur sporadically or in familial multiple tumor syndromes such as MEN1 (Multiple Endocrine Neoplasia type 1). Biallelic loss/inactivation of the MEN1 tumor suppressor gene is only found in 20–30% of sporadic pancreatic endocrine tumors. Therefore, identification of other molecular and genetic causes of pancreatic endocrine tumorigenesis is an area of intense investigation. Because MEN1 is the main gene reported so far that affects pancreatic endocrine tumors, analyzing downstream effects of menin ( MEN1 gene encoded protein) could uncover other candidate genes and pathways responsible for pancreatic endocrine tumorigenesis. During the process of endocrine pancreas development, a cascade of transcription factors under tight sequential- and temporal-regulated expression ensures normal organogenesis. Alteration of such developmental and differentiation factors could potentially lead to tumorigenesis.To study cellular transformation related to menin loss in the pancreatic β-cell, we used the mouse pancreatic β-cell line MIN6 as a model system. RNA and protein were isolated from MIN6 cells after menin knockdown or after menin over-expression as well as from their respective controls. Twelve transcription factors associated with β-cell differentiation were analyzed using QRT-PCR and western blot: Hlxb9, Hnf3β, Isl-1, MafA, MafB, NeuroD1, Ngn3, Nkx2.2, Nkx6.1, Pax4, Pax6 , and Pdx1 .Three different sources of menin siRNAs and four different transfection reagents were tested in time course knockdown experiments. Significant menin knockdown in MIN6 cells was observed with 74.3% ± 15.03% (n=6) knockdown efficiency at 72 hours post-transfection. For transient menin over-expression in MIN6 cells, the transfection efficiency was close to 60% (based on GFP plasmid transfection). Endogenous expression of all factors, except Ngn3 , was detectable in MIN6 cells. None of the eleven transcription factors showed significantly altered RNA expression upon menin knockdown or upon menin over-expression. Western blot analyses showed 4–5 factors that were up-regulated upon menin knockdown, and down-regulated upon menin over-expression. Evolutionarily conserved promoter regions of Hlxb9, Isl-1, Nkx6.1 , or Pax4 were not regulated upon menin knockdown or upon menin over-expression. These data indicate that menin could regulate some β-cell differentiation factors in a post-transcriptional manner. Mechanism of menin-mediated post-transcriptional regulation and downstream consequences on β-cell transformation and tumorigenesis is under investigation.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-140. doi:10.1158/1538-7445.AM2011-LB-140" @default.
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• W2313385191 date "2011-04-15" @default.
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• W2313385191 title "Abstract LB-140: Menin-mediated regulation of pancreatic β-cell differentiation factors" @default.
• W2313385191 doi "https://doi.org/10.1158/1538-7445.am2011-lb-140" @default.
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