Promyelocytic leukemia-specific PML-retinoic acid α receptor fusion protein interferes with erythRoid differentiation of human erythroleukemia K565 cells

Francesco Grignani, Ugo Testa, Marta Fagioli, Tiziano Barberi, Rosalba Masciulli, Gualtiero Mariani, Cesare Peschle, Pier Giuseppe Pelicci

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Abstract

Acute promyelocytic leukemia (APL) is characterized by a t(15;17) chromosomal translocation with breakpoints within the retinoic acid α receptor (RARα) gene on 17 and the PML gene, which encodes a putative transcription factor, on 15. A PML-RARα fusion protein is formed as a consequence of the translocation. We show here that expression of the PML-RARα protein in K562 erythroleukemia cells results in a reduced expression of erythroid differentiation markers and a reduced sensitivity to the erythroid differentiative action of heme. Overexpression of RARα, but not of PML, elicited a similar inhibition of K562 erythroid differentiation. These findings indicate that overexpression of either RARα or PML/RARα interferes with erythroid differentiation and support the hypothesis that RARα is involved in the regulation of normal hematopoiesis and alteration of the RARα signaling by PML/RARα is implicated in the promyelocytic leukemogenesis.

Original languageEnglish
Pages (from-to)440-443
Number of pages4
JournalCancer Research
Volume55
Issue number2
Publication statusPublished - Jan 15 1995

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ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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