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The antiproliferative effects of somatostatin receptor subtype 2 in breast cancer cells
Yong He1, Xiao-Mei Yuan, Ping Lei
1Department of Nuclear Medicine, Hubei Key Laboratory of Molecular Imaging, Union hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Aim:
Somatostatin receptor subtype 2 (SSTR2) is the principal mediator of somatostatin's (SST) antiproliferative effects on normal and cancer cells. Therefore, we investigated whether the enhanced expression of SSTR2 could inhibit the proliferation of tumor cells, and, if so, the mechanisms that might be involved.
Methods:
SSTR2 expression levels were determined by qRT-PCR in several tumor cell lines. Then, a plasmid pIRES2-EGFP-SSTR2 (pSIG) was constructed and stably transfected into MCF-7 cells (MCF-7/pSIG). After SSTR2 overexpression was identified by qRT-PCR, immunofluorescence staining and a receptor binding assay, the MCF-7/pSIG cells were analyzed by PI staining for apoptosis and cell cycle arrest was tested by flow cytometry for epidermal growth factor receptor (EGFR) expression. The EGF-stimulated proliferation of MCF-7 cells was assayed by MTT.
Results:
The human breast cancer cell line MCF-7 expresses a lower level of SSTR2, thereby partly accounting for the decreased response to SST. The overexpression of SSTR2 in MCF-7 cells resulted in apoptosis, cytostasis and G(1)/S cell cycle arrest. Furthermore, the expression of EGFR, together with EGF-stimulated proliferation, was markedly decreased in the MCF-7/pSIG cells.
Conclusion:
Enhanced SSTR2 expression played an antiproliferative role in MCF-7 cells through inducing apoptosis and G(1)/S cell cycle arrest, and also by decreasing EGFR expression, thereby counteracting the growth-stimulating effect of EGF. Our data seem to indicate that developing a new therapeutic agent capable of upregulating SSTR expression could potentially be a way to block tumor progression.Acta Pharmacologica Sinica (2009) 30: 1053-1059; doi: 10.1038/aps.2009.59.
Insights
Enhanced somatostatin receptor subtype 2 (SSTR2) expression inhibits tumor cell proliferation by inducing apoptosis and cell cycle arrest. This approach also reduces epidermal growth factor receptor (EGFR) expression, counteracting tumor growth signals.
Area of Science:
- Pharmacology
- Molecular Biology
- Cancer Research
Background:
- Somatostatin receptor subtype 2 (SSTR2) mediates somatostatin's (SST) antiproliferative effects.
- SSTR2 is crucial for inhibiting normal and cancer cell growth.
Purpose of the Study:
- To investigate if enhanced SSTR2 expression inhibits tumor cell proliferation.
- To elucidate the mechanisms underlying SSTR2-mediated tumor growth inhibition.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to assess SSTR2 levels in tumor cell lines.
- Stable transfection of MCF-7 cells with SSTR2-expressing plasmid (MCF-7/pSIG).
- Analysis of apoptosis, cell cycle, epidermal growth factor receptor (EGFR) expression, and proliferation via PI staining, flow cytometry, and MTT assays.
Main Results:
- MCF-7 cells exhibit low SSTR2 expression, correlating with reduced SST response.
- SSTR2 overexpression in MCF-7/pSIG cells induced apoptosis, cytostasis, and G(1)/S cell cycle arrest.
- EGFR expression and EGF-stimulated proliferation were significantly decreased in MCF-7/pSIG cells.
Conclusions:
- Enhanced SSTR2 expression exhibits antiproliferative effects in MCF-7 cells.
- Mechanisms include apoptosis induction, G(1)/S cell cycle arrest, and reduced EGFR expression.
- Upregulating SSTR expression may offer a therapeutic strategy to impede tumor progression.
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