Effects of combined octreotide and aspirin on the growth of gastric cancer.
- Author:
Chengwei TANG
1
;
Chunhui WANG
;
Liping TANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antineoplastic Combined Chemotherapy Protocols; therapeutic use; Aspirin; administration & dosage; Humans; Male; Mice; Mice, Inbred BALB C; Neoplasm Transplantation; Octreotide; administration & dosage; RNA, Messenger; analysis; Receptors, Somatostatin; genetics; Stomach Neoplasms; drug therapy; Transplantation, Heterologous
- From: Chinese Medical Journal 2003;116(3):373-377
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the effects of the combination of octreotide and aspirin on the growth of gastric cancer.
METHODSProliferation of gastric cancer cell lines treated with octreotide or aspirin was determined by (3)H-thymidine incorporation. After xenografts of human gastric cancer were implanted orthotopically in the stomach of nude mice, they were administered octreotide plus aspirin for 8 weeks. The mRNA of somatostatin receptor in the tissues of gastric carcinoma was detected by reverse transcription polymerase chain reaction (RT-PCR). Cyclooxygenase-2 in gastric cancer tissues was measured by immunohistochemistry.
RESULTSBoth octreotide and aspirin significantly reduced the (3)H-thymidine incorporation of gastric cancer cells. Xenografts in situ were found in all stomachs of nude mice except for two in the combination group. Either size or weight of tumors treated by octreotide, aspirin or in combination was significantly reduced as compared with that of controls. The inhibition rate for tumor was 60.6% (octreotide), 39.3% (aspirin), and 85.6% (in combination) respectively. No severe side effects were observed in any treated groups. Somatostatin receptor-2 and -3 were expressed in the transplanted gastric adenocarcinomas. Aspirin could down-regulate the strong expression of cyclooxygenase-2 in the tissue of gastric adenocarcinomas of nude mice.
CONCLUSIONA combination of octreotide and aspirin significantly inhibited proliferation of gastric cancer through mediation of somatostatin receptors and suppression of cyclooxygenase-2.