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Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

36.1K

The oncogenic E3 ligase TRIP12 suppresses epithelial-mesenchymal transition (EMT) and mesenchymal traits through

Kwok Kin Lee1, Deepa Rajagopalan2,3, Shreshtha Sailesh Bhatia2

  • 1Cancer Science Institute of Singapore, National University of Singapore, Singapore, 117599, Singapore. A0123884@u.nus.edu.

Cell Death Discovery
|May 8, 2021
PubMed

Insights

Thyroid hormone receptor interactor 12 (TRIP12) inhibits epithelial-mesenchymal transition (EMT), suppressing breast cancer metastasis. TRIP12 depletion promotes EMT and cellular motility, suggesting a tumor-suppressive role in metastasis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Oncology

Background:

  • Thyroid hormone receptor interactor 12 (TRIP12) is an E3 ligase known to degrade the tumor suppressor p14ARF.
  • TRIP12 is implicated in oncogenesis, but its role in cancer metastasis remains unexplored.
  • Understanding TRIP12's function in metastasis is crucial for developing novel cancer therapies.

Purpose of the Study:

  • To investigate the role of TRIP12 in breast cancer metastasis.
  • To elucidate the molecular mechanisms by which TRIP12 influences epithelial-mesenchymal transition (EMT).

Main Methods:

  • Analysis of publicly available cancer patient datasets.
  • TRIP12 depletion and ectopic expression studies in cell lines.
  • RNA sequencing (RNA-seq) to identify EMT-related gene expression changes.
  • Assessment of cellular phenotypes including polarity, adhesion, motility, and anoikis.

Main Results:

  • TRIP12 expression correlates with distant metastasis-free survival in breast cancer patients.
  • TRIP12 depletion induces EMT, characterized by altered cell adhesion markers, loss of polarity, and increased motility.
  • TRIP12 suppresses EMT by inhibiting ZEB1/2 gene expression; ZEB1/2 depletion reverses EMT phenotypes.
  • Ectopic TRIP12 expression sensitizes cells to anoikis, indicating a role in anoikis resistance.

Conclusions:

  • TRIP12 plays a significant role in suppressing EMT and inhibiting breast cancer metastasis.
  • TRIP12 acts by downregulating ZEB1/2 expression, thereby maintaining epithelial characteristics.
  • TRIP12 emerges as a potential therapeutic target for preventing breast cancer metastasis.

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