All-trans-retinoic acid induces CD52 expression in acute promyelocytic leukemia

Blood. 2003 Mar 1;101(5):1977-80. doi: 10.1182/blood-2002-05-1426. Epub 2002 Oct 17.

Abstract

It is well known that all-trans-retinoic acid (ATRA) can induce myeloid cell differentiation in acute promyelocytic leukemia (APL) cells. In this study, we found that ATRA treatment of the APL cell line NB4 induced the expression of CD52, both at transcriptional and translational levels. CD52 is a 21- to 28-kDa nonmodulating cell surface glycosylphosphatidylinositol-linked glycoprotein expressed on lymphocytes and monocytes, but not in human myeloid cells. The ATRA-dependent induction of CD52 expression was not observed in non-promyelocytic leukemia cell lines such as K562, U937, and HL-60, suggesting that induction of CD52 by ATRA may be specific to leukemic cells that express promyelocytic leukemia-retinoic acid receptor alpha (PML-RARalpha) or are at the promyelocytic stage of myeloid development. Antibodies against CD52 are used therapeutically against lymphocytes in certain leukemias and in patients undergoing transplantation. An ATRA-induced high level of CD52 expression might potentially serve as a novel therapeutic target in treatment of APL.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD / biosynthesis*
  • Antigens, CD / genetics
  • Antigens, Neoplasm / biosynthesis*
  • Antigens, Neoplasm / genetics
  • Antigens, Surface / biosynthesis
  • Antigens, Surface / genetics
  • Antineoplastic Agents / pharmacology*
  • CD52 Antigen
  • Cell Differentiation / drug effects
  • Gene Expression Regulation, Leukemic / drug effects*
  • Glycoproteins / biosynthesis*
  • Glycoproteins / genetics
  • HL-60 Cells / drug effects
  • HL-60 Cells / metabolism
  • Humans
  • K562 Cells / drug effects
  • K562 Cells / metabolism
  • Leukemia, Promyelocytic, Acute / genetics
  • Leukemia, Promyelocytic, Acute / pathology*
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism
  • Oncogene Proteins, Fusion / metabolism
  • Protein Biosynthesis / drug effects
  • Transcription, Genetic / drug effects
  • Tretinoin / pharmacology*
  • Tumor Cells, Cultured / drug effects
  • Tumor Cells, Cultured / metabolism
  • U937 Cells / drug effects
  • U937 Cells / metabolism

Substances

  • Antigens, CD
  • Antigens, Neoplasm
  • Antigens, Surface
  • Antineoplastic Agents
  • CD52 Antigen
  • CD52 protein, human
  • Glycoproteins
  • Neoplasm Proteins
  • Oncogene Proteins, Fusion
  • promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
  • Tretinoin