From the Ulubey Vocational School, Chemistry and Chemical Processing Technology Department, Laboratory Technology Program, Ordu, Turkey
Department of Medical Biochemistry, Karadeniz Technical University, Faculty of Medicine, Trabzon, Turkey.
QJM. 2016 Dec;109(12):785-790. doi: 10.1093/qjmed/hcw074. Epub 2016 Jun 1.
The purpose of this study was to determine whether irisin is secreted by gastric tumor cells experimentally induced in mice, and also if it has any effect on cancer cachexia.
12 out of 60 BALB/c mice were used as a control group, while N-nitroso-N-methylurea (MNU) was administered orally to the remaining 48. After 150 days, the surviving mice were sacrificed by decapitation, blood and stomach, skeletal muscle, brown and white adipose tissue specimens were collected. Following histopathological evaluation of the stomach tissues, it was decided to create four groups, one control group and three consisting of mice administered MNU, no cancer, pre-cancer and cancer. Gene expression analyses of fibronectin type III domain containing protein 5 (FNDC5) and some cachexia-related proteins were performed in tissue samples, while levels of irisin, and various inflammatory and tumor markers together with cachectic factors were determined in serum samples.
The levels of inflammatory, tumor markers and cachectic factors in serum samples were significantly higher in the cancer group compared with the control group. No expression of FNDC5 or zinc-α-2 glycoprotein, a cachectic factor, was observed in gastric tissues from the control and MNU groups, whereas significantly increased FNDC5 expression was determined in the both white and brown adipose tissues from the cancer group.
Increased FNDC5 expression in white and brown adipose tissues may have a cachectic effect in mice with induced cancer. However, it is not possible to explain the mechanism of the relationship between irisin and gastric cancer development on the basis of the results of this study.
本研究旨在确定胃肿瘤细胞是否在实验诱导的小鼠中分泌鸢尾素,以及鸢尾素是否对癌症恶病质有影响。
60 只 BALB/c 小鼠中有 12 只作为对照组,其余 48 只小鼠给予 N-亚硝基-N-甲基脲(MNU)口服。150 天后,通过断头法处死存活的小鼠,采集血液和胃、骨骼肌、棕色和白色脂肪组织标本。对胃组织进行组织病理学评估后,决定创建四个组,一个对照组和三个 MNU 组,分别为无癌、癌前和癌症。对纤维连接蛋白 III 型结构域包含蛋白 5(FNDC5)和一些恶病质相关蛋白进行组织样本基因表达分析,同时测定血清样本中的鸢尾素和各种炎症及肿瘤标志物以及恶病质因子的水平。
与对照组相比,癌症组血清样本中的炎症、肿瘤标志物和恶病质因子水平显著升高。对照组和 MNU 组的胃组织中均未观察到 FNDC5 或锌-α-2 糖蛋白(一种恶病质因子)的表达,而癌症组的白色和棕色脂肪组织中 FNDC5 的表达显著增加。
诱导癌症的小鼠白色和棕色脂肪组织中 FNDC5 表达的增加可能具有恶病质作用。然而,根据本研究的结果,尚无法解释鸢尾素与胃癌发展之间的关系机制。