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Retinoic acid regulates the expression of PBX1, PBX2, and PBX3 in P19 cells both transcriptionally and post‐translationally
Author(s) -
Qin Pu,
Haberbusch Juliet M.,
Soprano Kenneth J.,
Soprano Dianne Robert
Publication year - 2004
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20057
Subject(s) - retinoic acid , microbiology and biotechnology , retinoic acid inducible orphan g protein coupled receptor , p19 cell , biology , cancer research , gene , genetics , retinoic acid receptor , cellular differentiation , adult stem cell
Pre‐B cell leukemia transcription factors (PBXs) are important co‐factors for the transcriptional regulation mediated by a number of Hox proteins during embryonic development. It was previously shown that the expression of several Pbx genes is elevated in mouse embryo limb buds and embryonal carcinoma P19 cells upon retinoic acid (RA) treatment although the mechanism of this induction is not well understood. In this report, we demonstrate that PBX1a, PBX1b, PBX2, and PBX3 mRNAs and PBX1/2/3 proteins are induced during endodermal and neuronal differentiation of P19 cells in a RAR‐dependent subtype‐unspecific manner following RA treatment. The increases in both PBX1 mRNA and PBX3 mRNA levels are secondary responses to RA treatment requiring new proteins synthesis while the increase in PBX2 mRNA is a primary response. The RA‐dependent increases in PBX1 mRNA, PBX2 mRNA, and PBX3 mRNA levels are likely to be transcriptionally regulated since the stability of these mRNAs does not change. In addition, the half‐lives of PBX1/2/3 proteins are significantly extended by RA treatment. Two possible mechanisms could contribute to the stabilization of PBX proteins: PBX proteins associate with RA‐dependent increased levels of MEIS proteins, and RA may decrease the proteasome dependent degradation of PBX proteins. © 2004 Wiley‐Liss, Inc.