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Updated: Mar 29, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

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EDIL3/Del-1-Dependent Induction of AMPKβ Phosphorylation Regulates the Progression of Mesenchymal Stem-like

Seol-Hwa Jeong1, Soo Jung Lee2, In Hee Lee2

  • 1Cell & Matrix Research Institute, Kyungpook National University, Daegu 41944, Republic of Korea.

International Journal of Molecular Sciences
|March 28, 2026
PubMed

Insights

Developmental endothelial locus-1 (Del-1) promotes triple-negative breast cancer (TNBC) by activating AMPKβ, a key mediator driving tumor proliferation and invasion. Targeting AMPKβ may offer a new therapeutic strategy for aggressive TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Triple-negative breast cancer (TNBC) lacks targeted therapies, and the role of developmental endothelial locus-1 (EDIL3/Del-1) in its progression is unclear.
  • Understanding the molecular mechanisms driving TNBC is crucial for developing effective treatments.

Purpose of the Study:

  • To elucidate the role of Del-1 and AMP-activated protein kinase beta (AMPKβ) in TNBC.
  • To investigate the functional and mechanistic links between Del-1 and AMPKβ in TNBC progression.
  • To evaluate AMPKβ as a potential therapeutic target in TNBC.

Main Methods:

  • Profiling Del-1 and AMPK subunits in TNBC cell lines using RT-PCR and immunoblotting.
  • Functional assays in CRISPR/Cas9 Del-1 knockout and AMPKβ-manipulated cells.
  • Evaluating AMPKβ expression in early-stage TNBC tumors via tissue microarrays (TMA) and mRNA quantification.

Main Results:

  • Del-1 and AMPKβ were enriched in TNBC cells, particularly in the mesenchymal stem-like subtype.
  • Increased Del-1 and activated AMPKβ promoted TNBC cell proliferation and invasion.
  • Del-1 deletion suppressed tumor-promoting phenotypes by reducing AMPKβ expression.
  • Del-1 enhanced AMPKβ phosphorylation, amplifying oncogenic effects.
  • High AMPKβ protein expression correlated with poorer disease-free survival (DFS) in early TNBC patients.

Conclusions:

  • AMPKβ is a critical mediator of Del-1-driven signaling in TNBC.
  • AMPKβ plays a significant role in promoting TNBC proliferation and invasion.
  • AMPKβ represents a potential therapeutic target for aggressive TNBC subtypes.
Keywords:
AMP-activated protein kinase β subunitDel-1EDIL3triple-negative breast cancer

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