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Updated: Jun 15, 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
Inhibitory effect of octreotide on gastric cancer growth via MAPK pathway
Chun-Hui Wang1, Cheng-Wei Tang, Chun-Lun Liu
1Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China.
Aim:
Somatostatin and its analogues may suppress the growth of various tumor cells. However, the effect of octreotide on growth of gastric adenocarcinoma is still largely unknown. This study was to explore if octreotide could inhibit the growth of gastric adenocarcinoma and its probable mechanisms.
Methods:
Proliferation of gastric cancer cell line affected by octreotide was determined by (3)H-thymidine incorporation. After xenografts of human gastric cancer were implanted orthotopically in stomach, nude mice were administrated octreotide for 8 weeks. The mRNA of somatostatin receptor in the SGC-7901 cells was detected by reverse transcription polymerase chain reaction technique. Extracellular signal-regulated protein kinase and c-Fos in gastric cancer tissues were measured by immunohistochemistry and Western blot. Activator protein-1 binding activity was examined by electrophoretic mobility sift assay.
Results:
(3)H-thymidine incorporation into SGC-7901 cells was significantly decreased by octreotide in a concentration dependent manner. Either size or weight of tumors treated with octreotide was significantly reduced in vivo. The inhibition rate for tumor was 62.3 % in octreotide group. The genes of somatostatin receptors 2 and 3 were expressed in SGC-7901 gastric cancer cell lines. Extracellular signal-regulated protein kinase and c-Fos protein level were decreased in gastric adenocarcinoma treated with octreotide. Moreover, fetal calf serum stimulated activator protein-1 binding activity could be suppressed by octreotide potentially.
Conclusion:
Inhibition of sequential molecular events in MAPK pathway may interpret the mechanisms underlying the effect of octreotide on the growth of gastric adenocarcinoma.
Insights
Octreotide significantly inhibits gastric adenocarcinoma growth by impacting the MAPK pathway. This study reveals its potential as a therapeutic agent for gastric cancer by reducing tumor proliferation and key molecular signaling.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Somatostatin analogues show potential in suppressing various tumor cell growth.
- The specific impact of octreotide on gastric adenocarcinoma remains largely uninvestigated.
Purpose of the Study:
- To determine if octreotide inhibits gastric adenocarcinoma growth.
- To elucidate the probable mechanisms by which octreotide affects gastric cancer.
Main Methods:
- Assessed gastric cancer cell proliferation using (3)H-thymidine incorporation.
- Utilized orthotopic xenografts in nude mice treated with octreotide for 8 weeks.
- Analyzed somatostatin receptor mRNA, extracellular signal-regulated protein kinase (ERK), c-Fos protein levels, and activator protein-1 (AP-1) binding activity.
Main Results:
- Octreotide significantly reduced SGC-7901 cell proliferation in a dose-dependent manner.
- Tumor size and weight were significantly decreased in vivo, with a 62.3% inhibition rate.
- Octreotide decreased ERK and c-Fos protein levels and potentially suppressed AP-1 binding activity, with somatostatin receptors 2 and 3 expressed in cancer cells.
Conclusions:
- Octreotide demonstrates significant inhibitory effects on gastric adenocarcinoma growth.
- The mechanism involves the inhibition of sequential molecular events within the MAPK pathway.
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