Related Experiment Video
Updated: May 22, 2026

Establishing 3D Endometrial Organoids from the Mouse Uterus
Published on: January 6, 2023
Somatostatin and somatostatin analogues reduce PDGF-induced endometrial cell proliferation and motility
Marta Annunziata1, Raul M Luque, Mario Durán-Prado
1Laboratory of Molecular and Cellular Endocrinology, Department of Internal Medicine, University of Turin, Corso Dogliotti 14, 10126 Turin, Italy.
Background:
Endometriosis is characterized by ectopic implantation of endometrial cells, which show increased proliferation and migration. Somatostatin (SST) and its analogues inhibit normal and cancer cell growth and motility through the SST receptors, sst1-5. Cortistatin (CST), which displays high structural and functional homology with SST, binds all ssts, as well as MrgX2. Our objective was to investigate the gene expression of the SST/CST system and to determine the effect of SST and its analogues on platelet-derived growth factor (PDGF)-induced proliferation and motility in telomerase-immortalized human endometrial stromal cell (T HESC) line and in primary endometrial stromal cell (ESCs) isolated from human endometriotic tissues.
Methods:
Ectopic endometrial tissues were collected from women (n= 23) undergoing laparoscopic surgery for endometriosis (Stage III/IV). Gene expression was evaluated by real-time PCR, cell motility by wound healing assay, protein expression and β-actin rearrangement by immunofluorescence, cell proliferation by the Alamar blue assay and ERK1/2 and Akt phosphorylation by western blot.
Results:
Human endometriotic tissues, primary ESCs and T HESCs expressed SST, CST and ssts. SST, its analogues SOM230 and octreotide, as well as CST, counteracted PDGF-induced proliferation and migration in both ESCs and T HESCs. SST also inhibited vascular endothelial growth factor and metalloprotease-2 mRNA expression, and reduced basal and PDGF-induced ERK1/2 phosphorylation.
Conclusion:
These results indicate that the SST/CST system is expressed in endometriotic tissues and cells. The inhibitory effects of SST and its analogues on PDGF-induced proliferation and motility suggest that these peptides may represent promising tools in the treatment of endometriosis.
Insights
The somatostatin/cortistatin (SST/CST) system is present in endometriosis. SST and its analogues inhibit the proliferation and migration of endometrial stromal cells, suggesting potential therapeutic applications for endometriosis treatment.
Area of Science:
- Reproductive biology
- Endocrinology
- Molecular biology
Background:
- Endometriosis involves ectopic endometrial cell implantation, characterized by increased proliferation and migration.
- Somatostatin (SST) and Cortistatin (CST) are peptides that regulate cell growth and motility via SST receptors.
- The SST/CST system's role in endometriosis requires further investigation.
Purpose of the Study:
- To investigate the gene expression of the SST/CST system in endometriotic tissues and cells.
- To determine the effect of SST and its analogues on platelet-derived growth factor (PDGF)-induced proliferation and motility in endometrial stromal cells (ESCs).
Main Methods:
- Analysis of gene and protein expression of the SST/CST system in human endometriotic tissues, primary ESCs, and T HESCs.
- Assessment of cell proliferation using the Alamar blue assay.
- Evaluation of cell motility via wound healing assays and Western blotting for signaling pathway activation (ERK1/2, Akt).
Main Results:
- SST, CST, and their receptors were expressed in endometriotic tissues, primary ESCs, and T HESCs.
- SST, SOM230, octreotide, and CST inhibited PDGF-induced proliferation and migration in both cell types.
- SST reduced vascular endothelial growth factor and metalloprotease-2 mRNA expression and inhibited ERK1/2 phosphorylation.
Conclusions:
- The SST/CST system is expressed in endometriotic tissues and cells.
- SST and its analogues demonstrate inhibitory effects on endometrial stromal cell proliferation and motility.
- These findings suggest the SST/CST system as a potential therapeutic target for endometriosis.
Related Concept Videos
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Drugs Affecting GI Tract Motility: Dopamine Receptor Antagonists
Glucagon-like Receptor Agonists
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Mitogens and the Cell Cycle
Inhibition of Cdk Activity

