AMY-1 is a trigger for the erythrocyte differentiation of K562 cells

Int J Oncol. 2000 Feb;16(2):339-45. doi: 10.3892/ijo.16.2.339.

Abstract

We have reported that a novel c-Myc binding protein, AMY-1, stimulated the transcription activity of c-Myc and was translocated from cytoplasm to nuclei in a c-Myc-dependent manner. Here, the role of AMY-1 in cell differentiation was examined. AMY-1 expression was up-regulated after differentiation induction of human K562 cells to erythrocyte cells by AraC, while c-Myc expression was rapidly down-regulated. K562 cell lines expressing exogenous AMY-1 were established, and these cells expressed a high level of epsilon-globin mRNA, a marker gene necessary for erythrocyte cell differentiation, without differentiation induction. The addition of AraC rapidly initiated differentiation in these cell lines, which continued to differentiate to erythrocyte cells possessing a high level of hemoglobin even after the decrease in AMY-1 expression. These results suggest that AMY-1 is a trigger for K562 cells to differentiate to erythrocyte cells and that AMY-1 may have a function independent of or different from c-Myc.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antimetabolites, Antineoplastic / pharmacology
  • Cell Differentiation / physiology*
  • Cytarabine / pharmacology
  • DNA-Binding Proteins / physiology*
  • Globins / metabolism
  • Humans
  • K562 Cells / drug effects
  • K562 Cells / metabolism*
  • RNA, Messenger / metabolism*
  • Transcription Factors / physiology*

Substances

  • Antimetabolites, Antineoplastic
  • DNA-Binding Proteins
  • MYCBP protein, human
  • RNA, Messenger
  • Transcription Factors
  • Cytarabine
  • Globins