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Aplysin sensitizes cancer cells to TRAIL by suppressing P38 MAPK/survivin pathway

Jia Liu1, Leina Ma2, Ning Wu3

  • 1Institutes of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China. dadaliujia@gmail.com.

Marine Drugs
|September 27, 2014
PubMed

Insights

Aplysin, a marine compound, restores cancer cell sensitivity to tumor-necrosis factor-related apoptosis-inducing ligand (TRAIL) therapy by downregulating survivin. This compound shows promise for overcoming TRAIL resistance in cancer treatment.

Area of Science:

  • Oncology
  • Marine Natural Products Chemistry
  • Molecular Biology

Background:

  • Tumor-necrosis factor-related apoptosis-inducing ligand (TRAIL) induces cancer cell apoptosis but faces resistance.
  • Survivin overexpression is a key mechanism of TRAIL resistance in cancer cells.

Purpose of the Study:

  • To investigate Aplysin's potential to sensitize TRAIL-resistant cancer cells.
  • To elucidate the molecular mechanisms underlying Aplysin's TRAIL-sensitizing effects.

Main Methods:

  • In vitro and in vivo experiments using TRAIL-resistant cancer cell lines (A549, MCF7).
  • Assessment of apoptosis induction, survivin expression, and p38 MAPK activation.
  • Utilized p38 MAPK inhibitor (SB203580) to validate pathway involvement.

Main Results:

  • Aplysin restored TRAIL sensitivity in resistant cancer cells, enhancing apoptosis.
  • Aplysin treatment led to survivin downregulation.
  • Aplysin activated p38 MAPK, and its inhibition reversed Aplysin's TRAIL-sensitizing effects.

Conclusions:

  • Aplysin acts as a TRAIL sensitizer, potentially through the p38 MAPK/survivin pathway.
  • Aplysin demonstrates low cytotoxicity to normal cells, suggesting its utility in combination cancer therapy with TRAIL.

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