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GPR177 promotes gastric cancer proliferation by suppressing endoplasmic reticulum stress-induced cell death

Jaesung Seo1, Seung-H Lee1, Soo-Y Park1

  • 1Department of Biochemistry and Molecular Biology, Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seoul, Korea.

Journal of Cellular Biochemistry
|September 13, 2018
PubMed

Insights

This study shows endoplasmic reticulum (ER) stress can fight gastric cancer. Inhibiting GPR177 enhances chemotherapy, suggesting it as a therapeutic target for this common cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Gastric cancer is a leading global malignancy with limited effective chemotherapy options.
  • Overexpression of WLS1/GPR177 is linked to poor prognosis in gastric cancer patients.
  • GPR177 facilitates WNT ligand transport from the endoplasmic reticulum (ER) for secretion.

Purpose of the Study:

  • To investigate the anticancer effects of tunicamycin, an ER stress inducer, in gastric cancer.
  • To explore the role of GPR177 in gastric cancer cell response to ER stress and chemotherapy.

Main Methods:

  • Utilized tunicamycin to induce ER stress in gastric cancer cells.
  • Examined GPR177 expression levels and localization.
  • Employed small interfering RNA (siRNA) to knockdown GPR177.
  • Assessed apoptosis and cell proliferation using various treatments, including fluorouracil.

Main Results:

  • Tunicamycin downregulated GPR177 expression in a dose-dependent manner.
  • GPR177 knockdown sensitized gastric cancer cells to ER stress and tunicamycin-induced apoptosis.
  • GPR177 suppression enhanced the ER stress-mediated PERK-CHOP proapoptotic pathway.
  • Combination of fluorouracil and tunicamycin significantly reduced cancer cell proliferation.
  • Tunicamycin's efficacy was dependent on GPR177 expression levels.

Conclusions:

  • Endoplasmic reticulum stress can enhance anticancer effects in gastric cancer.
  • GPR177 plays a crucial role in gastric cancer cell survival under ER stress.
  • GPR177 represents a potential therapeutic target for improving gastric cancer chemotherapy.
Keywords:
WLS/GPR177apoptosisendoplasmic reticulum (ER)tunicamycinunfolded protein response

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