title: Cancer progenitors and epigenetic contexts: an Xisting connection.
abstract: In mammals, silencing of one of the two X chromosomes is necessary to achieve dosage compensation. The non coding RNA Xist triggers X inactivation. Gene silencing by Xist is only possible in certain developmental contexts that only exist in cells of the early embryo and specific hematopoietic progenitors. Critical silencing factors may only be present in these contexts giving an explanation of why Xist is not operative outside these contexts. It has been demonstrated that Xist is functional in tumor cells, where SATB1 was identified as the first silencing factor for Xist mediated chromosome silencing.
authors.affiliation: Research Institute of Molecular Pathology, Vienna, Austria. agrelo@imp.ac.at
authors.forename: Ruben
authors.initials: R
authors.lastname: Agrelo
authors.forename: Anton
authors.initials: A
authors.lastname: Wutz
mesh_terms: D000818:Animals; D004622:Embryo, Mammalian / Q000378:metabolism; D044127:Epigenesis, Genetic; D020868:Gene Silencing; D006412:Hematopoietic Stem Cells / Q000166:cytology / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics*; D014411:Neoplastic Stem Cells / Q000378:metabolism; D012313:RNA / Q000235:genetics; D022661:RNA, Untranslated / Q000235:genetics; D012097:Repressor Proteins / Q000235:genetics; D049951:X Chromosome Inactivation / Q000235:genetics*
chemical_list: D022661:RNA, Untranslated; D012097:Repressor Proteins; D012313:RNA