M Mohammadi1, M Hedayati1, N Zarghami2, S Ghaemmaghami2. 1. Shahid Beheshti University of Medical Sciences, Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Tehran, Islamic Republic of Iran. 2. Tabriz University of Medical Sciences, Division of Molecular Medicine, Department of Clinical Biochemistry, Tabriz, Islamic Republic of Iran.
Abstract
BACKGROUND: Resistin, as an adipokine, has been shown to be increased in serum plasma of gastric cancer patients and suggested to be a major factor in gastric carcinogenesis. However, it is still not clear how Resistin influences gastric cancer progression. The aim of this study was to evaluate Resistin effect on cell proliferation and expression of telomerase gene in gastric cancer cell line (AGS). METHODS: In this study, the proliferating activity of AGS cells stimulated with Resistin was also evaluated by using 2,3-Bis-(2-Methoxy-4-Nitro-5-Sulfophenyl)-2H-Tetrazolium-5-Carboxanilide (XTT) assay and trypan blue staining method. To investigate telomerase gene expression affected by Resistin, total RNA was extracted, cDNA was synthesized and expression of hTERT mRNA was carried out by real-time reverse transcription polymerase chain reaction. RESULTS: Exogenous Resistin has induced gastric cancer cells proliferation in a dose-dependent manner and could improve cell viability. Also the expression of Human Telomerase Reverse Transcriptase (hTERT) was upregulated in 24 hours, after Resistin treatment. CONCLUSIONS: This study has shown Resistin induces exogenously gastric cancer cell proliferation and increases hTERT gene expression. These findings may clarify the role of Resistin in gastric carcinogenesis. Therefore blocking Resistin signaling and limiting its secretion may be valuable for the treatment of gastric cancer.
BACKGROUND: Resistin, as an adipokine, has been shown to be increased in serum plasma of gastric cancer patients and suggested to be a major factor in gastric carcinogenesis. However, it is still not clear how Resistin influences gastric cancer progression. The aim of this study was to evaluate Resistin effect on cell proliferation and expression of telomerase gene in gastric cancer cell line (AGS). METHODS: In this study, the proliferating activity of AGS cells stimulated with Resistin was also evaluated by using 2,3-Bis-(2-Methoxy-4-Nitro-5-Sulfophenyl)-2H-Tetrazolium-5-Carboxanilide (XTT) assay and trypan blue staining method. To investigate telomerase gene expression affected by Resistin, total RNA was extracted, cDNA was synthesized and expression of hTERT mRNA was carried out by real-time reverse transcription polymerase chain reaction. RESULTS: Exogenous Resistin has induced gastric cancer cells proliferation in a dose-dependent manner and could improve cell viability. Also the expression of Human Telomerase Reverse Transcriptase (hTERT) was upregulated in 24 hours, after Resistin treatment. CONCLUSIONS: This study has shown Resistin induces exogenously gastric cancer cell proliferation and increases hTERT gene expression. These findings may clarify the role of Resistin in gastric carcinogenesis. Therefore blocking Resistin signaling and limiting its secretion may be valuable for the treatment of gastric cancer.
Authors: C M Steppan; S T Bailey; S Bhat; E J Brown; R R Banerjee; C M Wright; H R Patel; R S Ahima; M A Lazar Journal: Nature Date: 2001-01-18 Impact factor: 49.962
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