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BAP1 regulates AMPK-mTOR signalling pathway through deubiquitinating and stabilizing tumour-suppressor LKB1

Cong Yang1, Hongyu Ding2, Yang Yang2

  • 1Guizhou University School of Medicine, Guiyang, 550025, China.

Biochemical and Biophysical Research Communications
|August 22, 2020
PubMed

Insights

BRCA1-associated protein 1 (BAP1) stabilizes the tumor suppressor Liver kinase B1 (LKB1) by deubiquitination, impacting cell metabolism and proliferation. BAP1 deficiency may promote cancer cell growth and lipid synthesis.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Liver kinase B1 (LKB1) is a crucial tumor suppressor involved in cell survival, metabolism, and apoptosis.
  • BRCA1-associated protein 1 (BAP1) is a deubiquitinase with known roles in DNA repair and cell cycle regulation.

Purpose of the Study:

  • To investigate the interaction between BAP1 and LKB1.
  • To determine the functional consequences of BAP1-LKB1 interaction on cellular processes, including metabolism and proliferation.

Main Methods:

  • Yeast two-hybrid screening, co-immunoprecipitation, and GST pull-down assays to identify and confirm protein interactions.
  • Immunoblotting to assess the activation of downstream signaling pathways (AMPK, mTOR).
  • Cell survival assays, soft agar assays, qRT-PCR, and oil red O staining to evaluate proliferation and lipid synthesis.

Main Results:

  • BAP1 directly interacts with LKB1.
  • BAP1 deubiquitinates LKB1, inhibiting its degradation and stabilizing the protein.
  • BAP1 stabilization of LKB1 affects the activation of AMPK and downstream mTOR signaling.
  • BAP1 deficiency correlates with enhanced cancer cell proliferation and increased lipid synthesis.

Conclusions:

  • BAP1 plays a critical role in maintaining LKB1 stability and function.
  • The BAP1-LKB1 axis is a significant regulator of cellular metabolism and proliferation.
  • BAP1 deficiency represents a potential vulnerability in cancer that promotes uncontrolled cell growth and lipogenesis.
Keywords:
AMPKBAP1DeubiquitinationLKB1mTOR

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