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Updated: May 10, 2026

Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
Published on: January 22, 2018
Ghrelin induces gastric cancer cell proliferation, migration, and invasion through GHS-R/NF-κB signaling pathway
Chuang Tian1, Lianhai Zhang, Daohu Hu
1Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Gastrointestinal Surgery, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing, 100142, China.
Abstract:
This study aims to investigate the roles of ghrelin signaling in human gastric carcinoma cell lines AGS and SGC7901. Effects of ghrelin signaling on CDK6, P53, NF-κB/P65 and MMP2 mRNA and/or protein expression were determined by real-time PCR and western blot. MTT method and flow cytometry were performed to assess the gastric cancer cell proliferation. The SGC7901 cells overexpressing ghrelin were inoculated into nude mice to produce tumors which were measured later. The wound-healing assay and cell invasion assay were used to test the cell migration and invasive ability of gastric cancer. Ghrelin signaling promotes the oncogene CDK6 gene expression and represses the tumor suppressor gene P53 gene expression in gastric cancer. Ghrelin activates NF-κB/P65 signaling pathway through GHS-R in gastric cancer. Ghrelin upregulates the metastasis factor MMP2 expression via GHS-R/NF-κB signaling pathway in gastric cancer cells and promotes tumor cells migration and invasion, suggesting that ghrelin signaling is a critical pathway in cancer metastasis. Ghrelin induces cell proliferation, migration and invasion via GHS-R/NF-κB signaling pathway in gastric cancer cells. Ghrelin treatment must be avoided for gastric cancer patients.
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