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Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
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The phosphatase PPM1A inhibits triple negative breast cancer growth by blocking cell cycle progression

Abhijit Mazumdar1, William M Tahaney1,2, Lakshmi Reddy Bollu1

  • 11Department of Clinical Cancer Prevention, The University of Texas M.D. Anderson Cancer Center, Texas, USA.

NPJ Breast Cancer
|August 3, 2019
PubMed

Insights

Protein phosphatase Mg+2/Mn+2 dependent 1A (PPM1A) suppresses triple-negative breast cancer (TNBC) growth by blocking the cell cycle. Loss of PPM1A may predict sensitivity to CDK inhibitors in TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapy options.
  • Kinase signaling pathways are critical for TNBC growth, and phosphatases regulate these pathways.
  • Identifying differentially expressed phosphatases in ER-negative versus ER-positive breast cancers is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of protein phosphatase Mg+2/Mn+2 dependent 1A (PPM1A) in regulating TNBC growth.
  • To determine if PPM1A is differentially expressed in ER-negative breast cancers compared to ER-positive ones.
  • To explore PPM1A as a potential therapeutic target or predictive biomarker for TNBC.

Main Methods:

  • Examined PPM1A expression in ER-negative versus ER-positive breast cancers.
  • Assessed the effect of PPM1A deletion in ER-negative breast cancers.
  • Induced PPM1A expression in TNBC cells to evaluate its impact on in vitro and in vivo growth.
  • Analyzed PPM1A's effect on cell cycle progression, CDK, and Rb phosphorylation.

Main Results:

  • PPM1A is underexpressed in ER-negative breast cancers compared to ER-positive ones.
  • PPM1A is deleted in approximately 40% of ER-negative breast cancers.
  • Induced PPM1A expression suppressed both in vitro and in vivo growth of TNBC cells.
  • PPM1A induction blocked the cell cycle and reduced CDK and Rb phosphorylation.

Conclusions:

  • PPM1A is a critical regulator of cell cycle progression in triple-negative breast cancer.
  • PPM1A loss may serve as a predictive biomarker for sensitivity to CDK inhibitors in TNBC.
  • Targeting PPM1A or leveraging its loss as a biomarker holds promise for TNBC treatment strategies.
Keywords:
Breast cancerPredictive markers

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