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Expression of AdipoR1 and AdipoR2 and Serum Level of Adiponectin in Gastric Cancer

Background: Cancer is one of the major causes of death worldwide and the third leading cause of death in Iran. One of the proteins that are considered having anticancer effects is the adiponectin hormone. Adiponectin leads to programmed cell death, prevents cell growth and proliferation, and increas...

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Published in:Gastrointestinal Tumors 2020-10, Vol.7 (4), p.103-109
Main Authors: Kordafshari, Morteza, Nourian, Mahyar, Mehrvar, Narjes, Jalaeikhoo, Hassan, Etemadi, Aida, Khoshdel, Ali Reza, Idris, Mohammad Ghaznavi, Iravani, Shahrokh, Mehrvar, Azim
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Language:English
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Summary:Background: Cancer is one of the major causes of death worldwide and the third leading cause of death in Iran. One of the proteins that are considered having anticancer effects is the adiponectin hormone. Adiponectin leads to programmed cell death, prevents cell growth and proliferation, and increases the expression levels of BCL2. Aim: The aim of this study was to assay the expression of adiponectin receptors (AdipoR1 and AdipoR2) genes in gastric cancer patients. Materials and Methods: In this case-control study, 42 gastric cancer patients and 52 volunteers as healthy controls were enrolled. Total RNA was extracted. cDNA was synthesized by the reverse transcription method, and expression analysis was performed by real-time PCR. The serum level of adiponectin was also measured by ELISA. Results: The expression of both AdipoR1 and AdipoR2 was significantly higher than the control group (p = 0.02). Serum adiponectin was significantly lower in gastric cancer cases when compared with normal controls (p = 0.03). Conclusion: We found that expression level of AdipoR1 and AdipoR2 is strongly higher; however, the level of circulating adiponectin is lower in gastric cancer. Our study suggests that the expression of AdipoR1 and AdipoR2, besides the low level of adiponectin, may play an important role in the development and/or progression of gastric cancer.
ISSN:2296-3774
2296-3766
DOI:10.1159/000510342