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DEAR1, a novel tumor suppressor that regulates cell polarity and epithelial plasticity

Nanyue Chen1, Seetharaman Balasenthil1, Jacquelyn Reuther2

  • 1Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Cancer Research
|September 28, 2014
PubMed

Insights

The novel TRIM protein DEAR1 (TRIM62) regulates epithelial polarity and suppresses tumor-driving pathways like TGFβ-induced epithelial-mesenchymal transition (EMT). DEAR1 acts as a tumor suppressor and biomarker in breast cancer.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Epithelial plasticity is crucial for understanding metastasis and developing targeted therapies.
  • Identifying regulators of cell migration and invasion is key to preventing cancer spread.

Purpose of the Study:

  • To review the role of the TRIM protein DEAR1 (TRIM62) in regulating epithelial polarity, morphogenesis, and epithelial-mesenchymal transition (EMT).
  • To explore DEAR1's function as a tumor suppressor and its potential as a biomarker in epithelial cancers.

Main Methods:

  • Review of existing literature on DEAR1, TRIM proteins, and TGFβ signaling.
  • Analysis of DEAR1's interactions with SMAD3 and its downstream targets (SNAIL1/2).

Main Results:

  • DEAR1 regulates apical-basal polarity and acinar morphogenesis.
  • DEAR1 acts as a tumor suppressor on chromosome 1p35.
  • DEAR1 inhibits TGFβ-driven EMT by targeting SMAD3 and downregulating SNAIL1/2.
  • DEAR1 loss-of-function mutations and deletions are observed in epithelial cancers.

Conclusions:

  • DEAR1 plays a novel role in regulating the breast tumor microenvironment, polarity, and EMT.
  • DEAR1's alterations in cancer suggest its utility as a predictive/prognostic biomarker.
  • DEAR1 can stratify breast cancers for targeted therapies focused on its regulated pathways.

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