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Updated: Apr 15, 2026

Assessing Autophagic Flux by Measuring LC3, p62, and LAMP1 Co-localization Using Multispectral Imaging Flow Cytometry
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Published on: July 21, 2017

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AMBRA1 and BECLIN 1 interplay in the crosstalk between autophagy and cell proliferation

Valentina Cianfanelli1, Melania D'Orazio, Francesco Cecconi

  • 1a Unit of Cell Stress and Survival ; Danish Cancer Society Research Center ; Copenhagen , Denmark.

Cell Cycle (Georgetown, Tex.)
|March 25, 2015
PubMed

Insights

Autophagy proteins AMBRA1 and BECLIN 1 regulate the oncoprotein c-Myc stability. This interaction impacts cell proliferation and tumorigenesis, revealing new pathways in cancer research.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Autophagy-promoting proteins often inhibit cell proliferation.
  • AMBRA1 regulates the oncoprotein c-Myc stability via interaction with PP2A.
  • AMBRA1/PP2A activity is controlled by mTOR, a key regulator of cell growth.

Purpose of the Study:

  • To investigate the interplay between AMBRA1 and BECLIN 1 in regulating c-Myc.
  • To elucidate the distinct pathways through which AMBRA1 and BECLIN 1 influence c-Myc.
  • To determine if AMBRA1, BECLIN 1, and PP2A form a complex.

Main Methods:

  • Investigated protein interactions and regulatory pathways.
  • Analyzed the impact of AMBRA1 and BECLIN 1 on c-Myc stability and function.
  • Examined the formation of macromolecular complexes involving AMBRA1, BECLIN 1, and PP2A.

Main Results:

  • Both AMBRA1 and BECLIN 1 influence c-Myc regulation through separate pathways.
  • AMBRA1 and BECLIN 1, along with PP2A, form a macromolecular complex.
  • This complex formation suggests a coordinated role in c-Myc regulation.

Conclusions:

  • AMBRA1 and BECLIN 1 play distinct roles in c-Myc regulation.
  • These proteins co-exist within a macromolecular complex with PP2A.
  • Further studies are needed to understand the functional significance of this complex in autophagy and tumorigenesis.
Keywords:
EGFR degradationPP2Ac-Myccancercell cycle

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