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Updated: Aug 24, 2026
Generation of Orthotopic Pancreatic Tumors and Ex vivo Characterization of Tumor-Infiltrating T Cell Cytotoxicity
Published on: December 7, 2019
Characterization of somatostatin receptor expression in human pancreatic cancer using real-time RT-PCR
1Elkins Pancreas Center and Molecular Surgeon Research Center, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas 77030, USA.
Background:
Somatostatin inhibits cell proliferation and may act as a tumor suppressor by interacting with five different somatostatin receptors (SSTRs). We hypothesized that SSTR expression is down-regulated in human pancreatic cancer. In the current study, we used a powerful real-time RT-PCR technique to examine the mRNA expression levels of all five SSTR subtypes in human pancreatic cancer.
Materials And Methods:
Total RNA was extracted from three pancreatic cancer cell lines (Panc-1, MIA PaCa-2, and Hs 766T), three surgical specimens of pancreatic cancer, and adjacent pancreatic tissue, and a pancreatic cancer cell line transfected with the SSTR-2 gene. Specific primers were designed and mRNA levels for the five SSTRs were analyzed with real-time quantitative RT-PCR using a Bio-Rad iCycler system.
Results:
The pancreatic tumor specimens had a 2.5- and 4.3-fold reduction of SSTR-2 and SSTR-5 mRNA levels, respectively, as compared to their adjacent normal pancreatic tissues. SSTR-1 and SSTR-3 were also detected in both the cancer specimens and the adjacent tissues, but SSTR-4 was absent. Human pancreatic cancer cell lines also expressed SSTR-2 and SSTR-5 mRNA, but not SSTR-1, SSTR-3, and SSTR-4. Up-regulation of SSTR-2 mRNA by 2.2 x 10(4)-fold in Panc-1 cells resulted in receptor expression and growth inhibition.
Conclusion:
Expression of SSTR-2 and SSTR-5 could be important in the growth inhibitory effect of somatostatin in human pancreatic cancer. Down-regulation of SSTR transcription or SSTR mRNA instability may result in loss of a tumor suppressive effect of SSTRs in human pancreatic cancer.
Insights
Somatostatin receptors (SSTRs) are down-regulated in human pancreatic cancer, particularly SSTR-2 and SSTR-5. This loss may reduce somatostatin's tumor suppressive effects, impacting cancer growth.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Somatostatin inhibits cell proliferation and acts as a tumor suppressor.
- Five somatostatin receptors (SSTRs) mediate somatostatin's effects.
- SSTR expression is hypothesized to be reduced in human pancreatic cancer.
Purpose of the Study:
- To examine mRNA expression levels of all five SSTR subtypes in human pancreatic cancer.
- To investigate the role of SSTRs in pancreatic tumor growth.
Main Methods:
- Real-time RT-PCR was used to analyze SSTR mRNA expression.
- RNA was extracted from pancreatic cancer cell lines and surgical specimens.
- SSTR subtypes 1-5 mRNA levels were quantified.
Main Results:
- Pancreatic tumor specimens showed reduced SSTR-2 (2.5-fold) and SSTR-5 (4.3-fold) mRNA levels compared to normal tissue.
- SSTR-1 and SSTR-3 were detected in both tumor and normal tissues; SSTR-4 was absent.
- Pancreatic cancer cell lines expressed SSTR-2 and SSTR-5 mRNA, but not SSTR-1, SSTR-3, or SSTR-4.
Conclusions:
- SSTR-2 and SSTR-5 expression is crucial for somatostatin's growth inhibitory effects in pancreatic cancer.
- Down-regulation of SSTR transcription or mRNA instability may lead to the loss of tumor suppressive functions.
- Targeting SSTRs could be a therapeutic strategy for pancreatic cancer.
