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RECK regulated endoplasmic reticulum stress response and enhanced cisplatin-induced cell death in neuroblastoma cells

Yun Chen1, Ya-Hui Tsai, Sheng-Hong Tseng

  • 1Department of Surgery, Far Eastern Memorial Hospital, Pan-Chiao, New Taipei, Taiwan; Department of Chemical Engineering and Materials Science, Yuan Ze University, Chung-Li, Taoyuan, Taiwan.

Surgery
|October 3, 2013
PubMed
Abstract

Insights

Reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) interacts with GRP78 to regulate endoplasmic reticulum (ER) stress. RECK overexpression enhances cisplatin-induced neuroblastoma cell death, highlighting its role in cancer progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) is crucial for tumor cell invasion and metastasis.
  • The role of RECK in regulating the endoplasmic reticulum (ER) stress response is not well understood.

Purpose of the Study:

  • To identify proteins interacting with RECK.
  • To investigate the effects of RECK overexpression on the ER stress response.
  • To determine RECK's influence on cisplatin-induced cell death in neuroblastoma.

Main Methods:

  • Transfection of neuroblastoma cells with full-length RECK (FL-RECK) or a C-terminus-deleted mutant (del-C-RECK).
  • Immunoprecipitation (IP) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) to identify RECK-interacting proteins.
  • Western blot analysis to assess ER stress markers (PERK, eIF-2α phosphorylation) and apoptotic factors.

Main Results:

  • Glucose-regulated protein 78 (GRP78) was identified as a RECK-interacting protein, binding to the C-terminus of RECK.
  • FL-RECK overexpression, but not del-C-RECK, increased PERK and eIF-2α phosphorylation.
  • FL-RECK overexpression enhanced cisplatin-induced apoptosis and reduced cell viability by upregulating ER stress and apoptotic markers.

Conclusions:

  • RECK regulates the cellular ER stress response via interaction with GRP78.
  • RECK overexpression potentiates cisplatin-induced cell death in neuroblastoma.
  • RECK plays a significant role in modulating ER stress and chemosensitivity in cancer cells.

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