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.
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 humanpancreatic 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 humanpancreatic 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. Humanpancreatic 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 humanpancreatic cancer. Down-regulation of SSTR transcription or SSTR mRNA instability may result in loss of a tumor suppressive effect of SSTRs in humanpancreatic cancer.
Authors: Donghui Li; Motofumi Tanaka; F Charles Brunicardi; William E Fisher; Richard A Gibbs; Marie-Claude Gingras Journal: Cancer Date: 2011-01-10 Impact factor: 6.860
Authors: Aura D Herrera-Martínez; Manuel D Gahete; Sergio Pedraza-Arevalo; Rafael Sánchez-Sánchez; Rosa Ortega-Salas; Raquel Serrano-Blanch; Raúl M Luque; María A Gálvez-Moreno; Justo P Castaño Journal: Endocrine Date: 2017-12-01 Impact factor: 3.633
Authors: Muhammad Shahbaz; Fang Ruliang; Zhang Xu; Liang Benjia; Wang Cong; He Zhaobin; Niu Jun Journal: World J Surg Oncol Date: 2015-02-13 Impact factor: 2.754