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Prenylated Rab acceptor RABAC1 inhibits anti-apoptotic protein BCL2A1 and induces apoptosis

Jong-Tae Kim1, Hee Jun Cho1, Mi-Young Cho2

  • 1Immunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.

Biochemical and Biophysical Research Communications
|April 21, 2019
PubMed

Insights

Prenylated Rab acceptor 1 (RABAC1) inhibits the anti-apoptotic BCL2A1 protein, inducing apoptosis in gastric cancer cells. This finding suggests RABAC1 as a potential therapeutic target for BCL2A1-related cancers.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cell Death Research

Background:

  • The B cell lymphoma 2 (BCL2) family regulates apoptosis, with BCL2A1 conferring resistance to BCL2 inhibitors.
  • BCL2A1's anti-apoptotic activity makes it a potential target for anti-cancer therapies.

Purpose of the Study:

  • To investigate the role of prenylated Rab acceptor 1 (RABAC1) in regulating BCL2A1's anti-apoptotic function.
  • To determine if RABAC1 can induce apoptosis in gastric cancer cells.

Main Methods:

  • In vitro glutathione-S-transferase pull-down assay
  • Immunoprecipitation
  • Confocal microscopy
  • Caspase-3 activation assays
  • Cell proliferation, survival, migration, and invasion assays

Main Results:

  • RABAC1 directly interacts with BCL2A1.
  • RABAC1 inhibits BCL2A1's anti-apoptotic activity in AGS gastric cancer cells.
  • RABAC1 induces caspase-3 activation, decreasing cell proliferation, survival, migration, and invasion.
  • RABAC1 blocks BCL2A1's protective effect during cisplatin-induced apoptosis.

Conclusions:

  • RABAC1 effectively inhibits the anti-apoptotic protein BCL2A1.
  • RABAC1 induces apoptosis and reduces key cancer hallmarks in gastric cancer cells.
  • RABAC1 represents a promising therapeutic target for BCL2A1-associated cancers.
Keywords:
ApoptosisBCL2BCL2A1PRARABAC1

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