PML-Retinoic Acid Receptor α Inhibits PML IV Enhancement of PU.1-Induced C/EBPε Expression in Myeloid Differentiation | Zendy

Hitoshi Yoshida | Zendy; Hitoshi Ichikawa | Zendy; Yusuke Tagata | Zendy; Takuo Katsumoto | Zendy; Kazunori Ohnishi | Zendy; Yukihiro Akao | Zendy; Tomoki Naoe | Zendy; Pier Paolo Pandolfi | Zendy; Issay Kitabayashi | Zendy

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PML-Retinoic Acid Receptor α Inhibits PML IV Enhancement of PU.1-Induced C/EBPε Expression in Myeloid Differentiation

Author(s) -

Hitoshi Yoshida,

Hitoshi Ichikawa,

Yusuke Tagata,

Takuo Katsumoto,

Kazunori Ohnishi,

Yukihiro Akao,

Tomoki Naoe,

Pier Paolo Pandolfi,

Issay Kitabayashi

Publication year - 2007

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.02422-06

Subject(s) - retinoic acid , biology , acute promyelocytic leukemia , retinoic acid receptor , promyelocytic leukemia protein , transcription factor , retinoic acid receptor alpha , myeloid leukemia , myeloid , gene isoform , tretinoin , transcription (linguistics) , retinoic acid inducible orphan g protein coupled receptor , fusion protein , retinoic acid receptor gamma , cancer research , receptor , microbiology and biotechnology , cellular differentiation , biochemistry , gene , linguistics , philosophy , recombinant dna

PML and PU.1 play important roles in myeloid differentiation. PML-deficient mice have an impaired capacity for terminal maturation of their myeloid precursor cells. This finding has been explained, at least in part, by the lack of PML action to modulate retinoic acid-differentiating activities. In this study, we found that C/EBPepsilon expression is reduced in PML-deficient mice. We showed that PU.1 directly activates the transcription of the C/EBPepsilon gene that is essential for granulocytic differentiation. The type IV isoform of PML interacted with PU.1, promoted its association with p300, and then enhanced PU.1-induced transcription and granulocytic differentiation. In contrast to PML IV, the leukemia-associated PML-retinoic acid receptor alpha fusion protein dissociated the PU.1/PML IV/p300 complex and inhibited PU.1-induced transcription. These results suggest a novel pathogenic mechanism of the PML-retinoic acid receptor alpha fusion protein in acute promyelocytic leukemia.

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