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Phosphorylation of plectin by Akt3 promotes triple-negative breast cancer cell invasive migration

Shixue Zheng1,2, Chloe Chan1, John M Asara3

  • 1Tung Biomedical Sciences Centre and Department of Biomedical Sciences, College of Biomedicine, City University of Hong Kong, Kowloon, Hong Kong.

Iscience
|October 13, 2025
PubMed

Insights

Researchers identified a new signaling pathway involving Akt3 and plectin that drives triple-negative breast cancer (TNBC) growth and metastasis. Targeting this Akt3-plectin interaction may offer a novel therapeutic strategy for aggressive TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapies.
  • The PI3K/Akt pathway is crucial in cancer, but isoform-specific roles, especially for Akt3, remain unclear.
  • Akt3 is overexpressed in TNBC and linked to tumor progression.

Purpose of the Study:

  • To investigate the role of Akt3 in TNBC.
  • To identify Akt3 targets in TNBC cells.
  • To explore the therapeutic potential of targeting the Akt3 pathway in TNBC.

Main Methods:

  • Genome-wide proteomic screening to identify Akt3 substrates.
  • Functional assays to assess the impact of plectin depletion on TNBC cells.
  • Analysis of plectin phosphorylation and its effect on cell migration and invadopodia.

Main Results:

  • Plectin identified as an Akt3 substrate in TNBC.
  • Plectin depletion inhibits TNBC cell migration and invadopodia formation.
  • Akt3-mediated phosphorylation of plectin promotes TNBC cell migration via vimentin.

Conclusions:

  • Akt3 plays a significant role in promoting TNBC growth, stemness, and epithelial-mesenchymal transition.
  • The Akt3-plectin signaling axis is critical for TNBC cell migration and invadopodia formation.
  • Targeting Akt3-plectin signaling represents a promising therapeutic strategy for TNBC.
Keywords:
BiochemistryCancerProteomics

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