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Impacts of autophagy-inducing ingredient of areca nut on tumor cells

Ching-Yu Yen1, Wei-Fan Chiang2, Shyun-Yeu Liu1

  • 1Department of Dentistry, Taipei Medical University, Taipei, Taiwan; Department of Dentistry, National Defense Medical Center, Taipei, Taiwan; Oral and Maxillofacial Surgery Section, Chi Mei Medical Center, Tainan, Taiwan.

Plos One
|May 29, 2015
PubMed

Insights

Areca nut extract induces autophagic cell death through Beclin-1 and Atg5, with the MEK/ERK pathway involved. Long-term exposure may enhance tumor cell resistance to serum deprivation.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Autophagy Research

Background:

  • Areca nut (AN) is a widespread carcinogen linked to various cancers.
  • Previous studies showed AN extract (ANE) and its fraction (ANE 30-100K) induce autophagic cell death.
  • The precise molecular mechanisms of ANE-induced autophagy require further elucidation.

Purpose of the Study:

  • To investigate the detailed molecular mechanisms of ANE 30-100K-induced autophagy (AIA).
  • To explore the roles of AMP-activated protein kinase (AMPK), Beclin-1, Atg5, and the MEK/ERK pathway in AIA.
  • To assess the impact of long-term ANE 30-100K exposure on cancer cell resistance.

Main Methods:

  • Utilized chemical inhibitors and small hairpin RNA (shRNA) for gene knockdown (AMPK, Atg5, Beclin 1).
  • Examined AIA in various cancer cell lines (Jurkat T, OECM-1, CE81T/VGH, SCC25, SCC-15) and multiple myeloma/lymphoma cells.
  • Assessed caspase-3 activation and MEK/ERK pathway involvement.
  • Investigated cell resistance to serum deprivation after long-term ANE 30-100K treatment.

Main Results:

  • AMPK inhibition attenuated AIA in Jurkat T cells but not OECM-1 cells.
  • Knockdown of Atg5 and Beclin 1 significantly ameliorated AIA in tested cell lines.
  • ANE 30-100K activated caspase-3 upon Beclin 1 inhibition in specific cancer cells.
  • The MEK/ERK pathway was identified as an upstream activator of AIA in Jurkat T cells and involved in other cell lines.
  • Long-term ANE 30-100K treatment enhanced autophagy-mediated resistance to serum deprivation in surviving tumor cells.

Conclusions:

  • Beclin-1 and Atg5 are commonly required for AIA, while AMPK's role is cell-type specific.
  • The MEK/ERK signaling pathway plays a significant role in AIA.
  • Prolonged exposure to Areca nut extract may confer resistance to nutrient-deprived conditions in tumor cells, potentially impacting therapeutic outcomes.

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