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Somatostatin controls Kaposi's sarcoma tumor growth through inhibition of angiogenesis
A Albini1, T Florio, D Giunciuglio
1Modulo Progressione Neoplastica, Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy. albini@ermes.cba.uniga.it
Abstract:
Somatostatin and its analogs are active in the inhibition of SST receptor-positive endocrine neoplasms, but their activity and mechanism in nonendocrine tumors is not clear. Somatostatin potently inhibited growth of a Kaposi's sarcoma xenograft in nude mice, yet in vitro the tumor cells did not express any known somatostatin receptors and were not growth inhibited by somatostatin. Histological examination revealed limited vascularization in the somatostatin-treated tumors as compared with the controls. Somatostatin was a potent inhibitor of angiogenesis in an in vivo assay. In vitro, somatostatin inhibited endothelial cell growth and invasion. Migration of monocytes, important mediators of the angiogenic cascade, was also inhibited by somatostatin. Both cells types expressed somatostatin receptor mRNAs. These data demonstrate that somatostatin is a potent antitumor angiogenesis compound directly affecting both endothelial and monocytic cells. The debated function of somatostatin in tumor treatment and the design of therapeutic protocols should be reexamined considering these data.
Insights
Somatostatin effectively inhibits tumor growth by targeting angiogenesis, impacting endothelial and monocytic cells. This suggests a broader role for somatostatin in cancer therapy beyond endocrine tumors.
Area of Science:
- Oncology
- Endocrinology
- Angiogenesis Research
Background:
- Somatostatin analogs treat SST receptor-positive endocrine neoplasms.
- The role of somatostatin in nonendocrine tumors remains unclear.
- Kaposi's sarcoma is a nonendocrine tumor model.
Purpose of the Study:
- Investigate somatostatin's mechanism in nonendocrine tumor growth.
- Determine somatostatin's effect on angiogenesis.
- Explore somatostatin's impact on endothelial and monocytic cells.
Main Methods:
- Kaposi's sarcoma xenograft model in nude mice.
- In vitro studies on tumor cells, endothelial cells, and monocytes.
- Assessment of tumor vascularization and angiogenesis assays.
- Somatostatin receptor mRNA expression analysis.
Main Results:
- Somatostatin inhibited Kaposi's sarcoma xenograft growth.
- Tumor cells lacked known somatostatin receptors and were not directly inhibited.
- Reduced tumor vascularization observed in somatostatin-treated groups.
- Somatostatin inhibited angiogenesis in vivo and endothelial cell invasion in vitro.
- Somatostatin inhibited monocyte migration and affected both cell types expressing somatostatin receptor mRNAs.
Conclusions:
- Somatostatin acts as a potent anti-angiogenesis agent.
- It directly impacts endothelial and monocytic cells, mediating antitumor effects.
- Reevaluation of somatostatin's therapeutic role in nonendocrine tumors is warranted.