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Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
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Ghrelin Regulates Cyclooxygenase-2 Expression and Promotes Gastric Cancer Cell Progression

Huanqing Li1, Xiaohong Zhang1, Li Feng1

  • 1Endoscopy Center, Minhang District Central Hospital of Fudan University, Shanghai, China.

Computational and Mathematical Methods in Medicine
|June 14, 2021
PubMed
Abstract

Insights

Ghrelin promotes gastric cancer cell migration and invasion while inhibiting apoptosis by targeting the PI3K/Akt/COX-2 pathway. This research identifies ghrelin as a potential molecular target for gastric cancer treatment.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Signaling

Background:

  • Gastric cancer (GC) remains a significant global health challenge.
  • Understanding the molecular mechanisms driving GC progression is crucial for developing effective therapies.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which ghrelin influences apoptosis, migration, and invasion in gastric cancer cells.
  • To investigate the role of the PI3K/Akt/COX-2 pathway in ghrelin-mediated GC cell behavior.

Main Methods:

  • Gastric cancer AGS cells were treated with ghrelin, a cyclooxygenase-2 inhibitor (NS398), and an Akt inhibitor (perifosine).
  • Apoptosis was assessed using TUNEL and flow cytometry assays.
  • Protein expression of PI3K, p-Akt, and COX-2 was analyzed via Western blot.
  • Cell migration and invasion were evaluated using wound-healing and Transwell assays.

Main Results:

  • Ghrelin treatment increased cell migration and invasion while decreasing apoptosis rates in GC cells.
  • Ghrelin elevated the protein expression of p-Akt, PI3K, and COX-2.
  • Inhibition of Akt or COX-2 partially reversed ghrelin's effects on protein expression and cell behavior.

Conclusions:

  • Ghrelin regulates gastric cancer cell migration, invasion, and apoptosis by targeting the PI3K/Akt/COX-2 signaling pathway.
  • Ghrelin upregulates COX-2 expression in GC cells via PI3K/Akt signaling.
  • Ghrelin presents a potential molecular target for therapeutic intervention in gastric cancer.

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