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Myosin 1b Regulates Nuclear AKT Activation by Preventing Localization of PTEN in the Nucleus

Yi Yu1, Yuyan Xiong1, Diogo Ladeiras1

  • 1Cardiovascular and Aging Research, Department of Endocrinology, Metabolism and Cardiovascular System, Medicine Section, Faculty of Science and Medicine, University of Fribourg, Chemin du Musée 5, 1700 Fribourg, Switzerland.

Iscience
|July 27, 2019
PubMed

Insights

Myosin 1b (MYO1B) interacts with PTEN, preventing its nuclear entry. This interaction promotes nuclear AKT activation, suppressing apoptosis and offering potential therapeutic strategies for melanoma.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Insulin signaling pathways, including AKT activation, are crucial in cellular processes.
  • Phosphatidylinositol 3-kinase (PI3K) and phosphatase and tensin homolog (PTEN) are key regulators of AKT.
  • Myosin 1b (MYO1B) has been implicated in regulating other signaling pathways, but its role in AKT activation is unclear.

Purpose of the Study:

  • To investigate the role of Myosin 1b (MYO1B) in insulin-induced AKT activation.
  • To determine the interaction between MYO1B and PTEN and its effect on nuclear PTEN localization.
  • To elucidate the impact of MYO1B-PTEN interaction on cellular apoptosis.

Main Methods:

  • Silencing MYO1B in mouse embryonic fibroblasts (MEFs).
  • Co-immunoprecipitation, co-immunostaining, and proximity ligation assays to assess protein interactions.
  • Analysis of nuclear and cytoplasmic AKT and PTEN levels.
  • Assessment of apoptosis in MEFs and melanoma B16F10 cells.

Main Results:

  • Silencing MYO1B inhibited nuclear AKT activation and increased nuclear PTEN levels.
  • MYO1B directly interacts with PTEN, reducing its nuclear accumulation.
  • Elevated nuclear PTEN due to MYO1B silencing promoted apoptosis in MEFs and melanoma cells.

Conclusions:

  • MYO1B interacts with PTEN, inhibiting its nuclear localization and facilitating nuclear AKT activation.
  • This interaction suppresses apoptosis, suggesting MYO1B's role in cell survival.
  • Targeting the MYO1B-PTEN interaction could offer a novel therapeutic strategy for cancers like melanoma.
Keywords:
BiochemistryBiological SciencesCell BiologyMolecular Biology

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