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Resistin and Visfatin Expression in HCT-116 Colorectal Cancer Cell Line
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Sara Ghaemmaghami1   , Seyed Mojtaba Mohaddes 2, Mehdi Hedayati3 , Masume Gorgian Mohammadi1 , Golnoosh Dehbashi3 |
1- Department of Clinical Biochemistry, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
2- Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. , mohaddesmo@yahoo.com
3- Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. |
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Abstract: (16980 Views) |
| Adipocytokines, hormones secreted from adipose tissue, have been shown to be associated with many cancers such as breast, prostate and colorectal cancer. Recent studies have indicated that resistin and visfatin, two of these adipokines have high level plasma concentrations in colorectal cancer patients and may be promising biomarkers for colorectal cancer. The aim of this study was to identify whether the colorectal cancer cell line, HCT-116, itself is the source of these two adipokines secretion. Resistin and visfatin expression were investigated in HCT-116 by RT – PCR at mRNA level and confirmed by ELISA at protein level. Visfatin showed a high expression at both mRNA and protein levels in HCT-116. Conversely, resistin was not expressed in either cell lysate or supernatant. These results showed that HCT-116 colorectal cancer cells secrete and express visfatin endogenously. However, they are not the main source of resistin and the high level of resistin in colorectal cancer may be due to monocytes and other inflammatory cells which increase in proinflammation status of cancer. Taken together, visfatin may act on colorectal cancer cell in an autocrine manner while resistin may act in a paracrine manner. |
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| Keywords: Visfatin, resistin, colorectal cancer |
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Full-Text [PDF 145 kb]
(3990 Downloads)
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Type of Study: Original Article |
Subject:
Cancer
Received: 2013/06/9 | Accepted: 2013/08/28 | Published: 2013/08/28
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