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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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Cis-acting Elements involved in mRNA stability
mRNA Stability and Gene Expression02:51

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IL-3 and oncogenic Abl regulate the myeloblast transcriptome by altering mRNA stability.

Jason Ernst1, Louis Ghanem, Ziv Bar-Joseph

  • 1Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Boston, Massachusetts, USA.

Plos One
|October 16, 2009
PubMed
Summary

Interleukin-3 (IL-3) stabilizes hundreds of messenger RNA (mRNA) transcripts, influencing myeloblast function and potentially contributing to leukemia. This posttranscriptional regulation highlights a new mechanism in cell growth control.

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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

Area of Science:

  • Molecular Biology
  • Hematology
  • Cancer Research

Background:

  • Interleukin-3 (IL-3) is a growth factor crucial for hematopoietic progenitor survival and myelopoiesis.
  • IL-3's role in opposing granulopoiesis and supporting leukemia growth is known, but its posttranscriptional mechanisms remain unclear.
  • Understanding IL-3's impact on mRNA stability is key to deciphering its role in normal hematopoiesis and leukemogenesis.

Purpose of the Study:

  • To investigate the posttranscriptional effects of Interleukin-3 (IL-3) on mRNA stability in myeloblasts.
  • To identify specific mRNA targets and regulatory elements involved in IL-3-mediated transcript stabilization.
  • To explore the connection between IL-3-induced mRNA stabilization and leukemic cell growth.

Main Methods:

  • Global mRNA decay profiling and bioinformatic analyses were performed on 32Dcl3 myeloblasts.
  • Identification and characterization of AU-Response elements (AREs) in IL-3-stabilized transcripts.
  • Functional assays using an interleukin-6 (IL-6) 3'-UTR domain to assess IL-3 responsiveness.

Main Results:

  • IL-3 rapidly stabilized hundreds of transcripts crucial for myeloblast function.
  • Stabilized transcripts were significantly enriched for AU-Response elements (AREs).
  • An ARE-containing domain from IL-6 conferred IL-3 responsiveness to a heterologous gene, confirming a role for AREs in IL-3-mediated stabilization.
  • Many IL-3-stabilized transcripts are implicated in leukemic transformation.
  • Deregulated Abl kinase and IL-3 share the ability to delay transcript turnover, partly via Mek/Erk signaling.

Conclusions:

  • IL-3 regulates cellular processes primarily through the control of mRNA stability.
  • Aberrant stabilization of an IL-3-associated mRNA network contributes to leukemic cell proliferation.
  • These findings reveal a novel mechanism of IL-3 action with implications for understanding and treating myeloid leukemias.