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The protein phosphatase 2A regulatory subunit B55α is a modulator of signaling and microRNA expression in acute

Peter P Ruvolo1, Vivian R Ruvolo1, Rodrigo Jacamo1

  • 1Division of Molecular Hematology, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Biochimica Et Biophysica Acta
|May 27, 2014
PubMed

Insights

Protein phosphatase 2A (PP2A) B55α subunit (PPP2R2A) under-expression in acute myeloid leukemia (AML) correlates with poor outcomes. Loss of B55α activates pathways supporting leukemia cell survival.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Biology

Background:

  • The protein phosphatase 2A (PP2A) B55α subunit (PPP2R2A) is significantly under-expressed in acute myeloid leukemia (AML) blast cells.
  • This down-regulation of B55α is associated with a shorter remission duration in AML patients.

Purpose of the Study:

  • To investigate the functional role of the PP2A B55α subunit in AML.
  • To identify proteins and pathways regulated by B55α in AML.

Main Methods:

  • Reverse phase protein analysis (RPPA) of 230 proteins in 511 AML patient samples.
  • ShRNA-mediated suppression of B55α in OCI-AML3 AML cells.
  • Analysis of PP2A isoform activity, MYC stoichiometry, and microRNA expression.

Main Results:

  • B55α expression strongly correlates with MYC, PKCα, and SRC levels.
  • B55α functions as a PKCα phosphatase, while SRC suppresses B55α expression.
  • Loss of B55α leads to MYC suppression and induction of the B56α isoform, altering microRNA profiles (miR-191-5p up, miR-142-3p down).

Conclusions:

  • Suppression of B55α in AML activates signaling pathways that promote leukemia cell survival.
  • B55α levels are critical for regulating cellular pathways and microRNA expression in AML.
  • Targeting B55α or its downstream effectors may offer therapeutic strategies for AML.
Keywords:
AMLB55αCell signalingRelapsemiR-142miR-191

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