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

Research output: Contribution to journalArticle


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
Issue number2
Publication statusPublished - Jan 15 1995


ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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