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Phosphodiesterase 7B/microRNA-200c relationship regulates triple-negative breast cancer cell growth

Dan-Dan Zhang1, Yue Li2, Yuan Xu3

  • 1Institute of Interdisciplinary Integrative Medical Research, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China. izhangdd@126.com.

Oncogene
|September 14, 2018
PubMed

Insights

MicroRNA-200c (miR-200c) inhibits triple-negative breast cancer (TNBC) growth by targeting phosphodiesterase 7B (PDE7B), distinct from its known EMT role. This interaction elevates cAMP levels, promoting apoptosis and potentially improving patient survival.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • MicroRNA-200 (miRNA-200) family members regulate epithelial-to-mesenchymal transition (EMT) by suppressing Zeb1 and Zeb2.
  • Hsa-miR-200c-3p (miR-200c), a member of the miRNA-200 family, is underexpressed in triple-negative breast cancer (TNBC) and inhibits cell migration.
  • The precise mechanism of miR-200c's role in TNBC growth inhibition beyond EMT suppression requires elucidation.

Purpose of the Study:

  • To investigate the mechanism by which miR-200c inhibits TNBC cell growth and tumor development.
  • To identify novel targets of miR-200c involved in TNBC pathogenesis.
  • To explore the therapeutic potential of the miR-200c/target interaction in TNBC.

Main Methods:

  • Utilized cell culture models of TNBC and ectopic miR-200c expression.
  • Performed gene silencing (siRNA) and overexpression (transgene) experiments for miR-200c and its targets.
  • Quantified intracellular cAMP levels and assessed apoptosis and cell cycle arrest.
  • Analyzed patient tumor gene expression datasets for correlation analysis.

Main Results:

  • miR-200c potently inhibited TNBC cell growth and tumor development through a mechanism independent of Zeb1/Zeb2 downregulation.
  • Phosphodiesterase 7B (PDE7B) was identified as a direct target of miR-200c, mediating its tumor-suppressive effects.
  • miR-200c increased intracellular cAMP levels in TNBC cells, leading to apoptosis and cell cycle arrest.
  • Low miR-200c and high PDE7B expression correlated with poor patient survival in breast cancer datasets.

Conclusions:

  • miR-200c inhibits TNBC cell growth and tumor development by targeting PDE7B mRNA, leading to elevated cAMP levels and apoptosis.
  • The miR-200c/PDE7B axis represents a novel regulatory pathway in TNBC tumorigenesis.
  • This pathway holds potential as a therapeutic target for improving outcomes in breast cancer patients, particularly those with TNBC.

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