RESUMEN
Objective To explore the influence of low-selenium diet on expression of selenium-binding protein 1 (SBP1) and selenoprotein P (Sel P) in liver,kidney and brain tissues.Methods C57BL/6 mice were randomly divided into four groups according to body weight:control group,low-selenium treatment for 4-,12-and 24-week groups,10 mice in each group,half male and half female.The control group was fed with normal diet (selenium content was 0.300 mg/kg),distilled water,and sacrificed at the 12th week; low-selenium treatment groups were fed with low-selenium diet(selenium content was 0.015 mg/kg),then sacrificed at the 4th,12th and 24th weeks,respectively.Expressions of SBP1 and Sel P in mouse liver,kidney and brain tissues were determined by Western blotting.Results Expressions of SBP1 and Sel P in low-selenium feed mouse liver tissue at the 4th,12th and 24th weeks were,respectively,as follows 0.11 ± 0.01,0.36 ± 0.01,0.59 ± 0.02 and 0.41 ± 0.01,0.39 ± 0.02,0.25 ± 0.02;in kidney,respectively,as follows 0.60 ± 0.03,0.20 ± 0.02,0.03 ± 0.01 and 0.88 ± 0.01,0.73 ± 0.03,0.85 ± 0.02; in brain,respectively,as follows 0.54 ± 0.03,0.11 ± 0.01,0.01 ± 0.01 and 0.50 ± 0.02,0.49 ± 0.03,0.38 ± 0.02.Expression of Sel P in low-selenium feed mouse liver,kidney and brain tissues was significantly decreased as compared to that of control group(1.00 ± 0.00,1.00 ± 0.00,all P ＜ 0.05),but SBP1 content was reduced at first and then rebounded in kidney,and was in decreasing trend in liver and brain tissues.Conclusion Low-selenium diet has a certain effect on expression of SBP1 and Sel P in mouse liver,kidney and brain tissues.
RESUMEN
Objective To detect the expression of selenium binding protein 1 ( SBP1 ) in gastric cancer cell line SGC7901, BGC823, normal gastric epithelial cell line GES-1, gastric cancer tissues and normal gastric tissues, explore the relationship between SBP1 and pathologic features, and discuss the feasibility of SBP1 as an diagnostic marker of gastric cancer. Methods The clinical data of 135 patients with gastric cancer who were admitted to Zhongnan Hospital of Wuhan University from 2006 to 2007 were retrospectively analyzed. The expression of SBP1 in the gastric cancer tissues and 16 cases of normal gastric tissues were detected by immunohistochemistry. The mRNA and protein expressions of SBP1 of SGC7901, BGC823 and GES-1 were determined by Western blot and RT-PCR. All data were analyzed by using chi-square test and one-way analysis of variance.Results The mRNA expressions of SBP1 in BGC823 and SGC7091 were 0. 120 ± 0. 020 and 0. 133 ± 0. 015,respectively, which were significantly lower than 0. 907 ± 0. 015 in GES-1 ( F = 2106. 462, P ＜ 0.05 ). The protein expression of SBP1 in BGC823 and SGC7901 were 0.253 ±0.015 and 0.273 ±0.015 ,respectively, which were significantly lower than 0.877 ±0.025 in GES-1 ( F = 1026. 758, P ＜0.05 ). A strong positive reaction of SBP1 was observed in 3 cases of gastric cancer tissues and 16 cases of normal gastric tissues. The decrease of the protein expression of SBP1 was correlated with clinical stages of the patients ( x2 = 12. 629, P ＜ 0.05 ), rather than the sexes, ages, tumor histological types, tumor differentiation, infiltration depths and lymph node metastasis (x2 =2. 142, 0.860, 1.838, 5.001,4.858, 1.994, P＞0. 05). Conclusions The decrease of SBP1 expression could be used as a marker in diagnosing gastric cancer. Down-regulation of SBP1 expression may play an important role in the genesis and prognosis of gastric cancer.
RESUMEN
BACKGROUND: Human selenium binding protein 1 (SELENBP1) is a protein that binds selenium as a cofactor. The decreased expression of SELENBP1 in several types of carcinomas and its association with a poor prognosis have previously been reported on. In this study, we evaluated the expression of SELENBP1 in low-grade and high-grade epithelial dysplasia/ adenomas and adenocarcinomas. METHODS: We analyzed 45 cases of low-grade epithelial dysplasia/adenomas, 42 cases of high-grade epithelial dysplasia/adenomas and 64 cases of adenocarcinomas and all of them were obtained from endoscopic mucosal resection or endoscopic submucosal dissection. We analyzed all of them for their SELENBP1 expression by immunohistochemistry. Eight triple-paired cases of gastric mucosa, adenoma and adenocarcinoma from the same patient were selected for RT-PCR analysis. RESULTS: There was a progressive decrease in the expression of SELENBP1 from the low-grade dysplasia/adenomas (42/45, 93%) to the high-grade dysplasia/adenomas (29/42, 69%) and finally to the adenocarcinomas (24/64, 37%), (p<0.001). The progressive decrease in the SELENBP1 expression was also evident in the eight paired cases that were analyzed by RT-PCR. CONCLUSIONS: Our findings demonstrate that the SELENBP1 expression is suppressed in gastric epithelial dysplasia/adenomas and adenocarcinomas. The suppression of SELENBP1 was significantly more frequent and severer in the adenocarcinomas than that in the low-grade dysplasia/ adenomas, and this implies that the suppression of SELENBP1 is a late event in gastric carcinogenesis.