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RECK/GPR124-driven WNT signaling in pancreatic and gastric cancer cells

Hai Yu1, Susumu Kohno1, Dominic Chih-Cheng Voon2

  • 1Division of Oncology and Molecular Biology, Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan.

Cancer Science
|June 26, 2024
PubMed

Insights

Reversion-inducing cysteine-rich protein withkazal repeats (RECK) promotes cancer growth by enhancing WNT signaling via GPR124. Targeting the RECK/GPR124 complex may offer new therapeutic strategies for pancreatic and gastric cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Reversion-inducing cysteine-rich protein with kazal repeats (RECK) regulates extracellular matrix components and has been linked to G protein-coupled receptor 124 (GPR124) in non-tumor contexts.
  • The precise role of RECK in cancer cell WNT signaling remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of RECK in promoting WNT signaling and tumor growth in cancer cells.
  • To determine the functional interaction between RECK and GPR124 in cancer.

Main Methods:

  • Co-immunoprecipitation assays to confirm RECK and GPR124 complex formation.
  • WNT signaling pathway activity assays in cell lines with varying RECK and GPR124 expression.
  • Cell proliferation and apoptosis assays following genetic manipulation of RECK and GPR124.

Main Results:

  • RECK and GPR124 form a complex that significantly enhances WNT signaling in a WNT7-dependent manner.
  • RECK promotes the growth of KRAS-mutated pancreatic ductal adenocarcinoma (PDAC) cells, dependent on GPR124.
  • Depletion of GPR124 in gastric cancer cells led to more pronounced inhibition of cell growth and WNT signaling than RECK depletion.

Conclusions:

  • RECK positively modulates WNT signaling through GPR124, thereby promoting tumor cell growth.
  • The RECK/GPR124 complex represents a potential therapeutic target for pancreatic ductal adenocarcinoma and gastric cancer.
Keywords:
GPR124RECKWNT7gastric cancerpancreatic cancer

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