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The proliferative effects of ghrelin on human gastric cancer AGS cells

Pei Ying Tian1, Xiao Ming Fan

  • 1Department of Gastroenterology, Jinshan Hospital, Fudan University, Shanghai Medical College of Fudan University, Shanghai, China.

Journal of Digestive Diseases
|August 23, 2012
PubMed
Abstract

Insights

Ghrelin and des-acyl ghrelin stimulate gastric cancer cell proliferation by activating the ERK1/2 and PI3K/Akt pathways. These findings highlight potential therapeutic targets for gastric cancer treatment.

Area of Science:

  • Gastroenterology and Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Ghrelin, a peptide hormone, plays a role in various physiological processes.
  • Gastric cancer remains a significant global health concern with complex underlying mechanisms.
  • Understanding the molecular pathways involved in gastric cancer cell growth is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the effect of ghrelin and its derivative, des-acyl ghrelin, on gastric cancer cell proliferation.
  • To elucidate the signaling pathways, specifically ERK1/2 and PI3K/Akt, involved in ghrelin-mediated gastric cancer cell growth.
  • To identify potential molecular targets for gastric cancer treatment.

Main Methods:

  • Gastric cancer cell line (AGS) proliferation was assessed using MTT assays.
  • Gene expression of growth hormone secretagogue receptors (GHS-R1a and GHS-R1b) was analyzed via RT-PCR.
  • Western blotting was employed to measure the activation of ERK1/2 and Akt signaling pathways.
  • Flow cytometry was used to analyze cell cycle distribution.

Main Results:

  • AGS cells expressed both GHS-R1a and GHS-R1b mRNA.
  • Ghrelin and des-acyl ghrelin significantly increased AGS cell proliferation at specific concentrations (1 and 10 nmol/L).
  • Ghrelin and des-acyl ghrelin activated the ERK1/2 and Akt signaling pathways, leading to cell cycle progression into the S phase.

Conclusions:

  • Ghrelin and des-acyl ghrelin promote gastric cancer cell proliferation.
  • The proliferative effect is mediated through the activation of the ERK1/2 and PI3K/Akt signaling pathways.
  • These findings suggest that ghrelin signaling could be a potential therapeutic target in gastric cancer.

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