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Objective To investigate the expression of S100A16 in pancreatic cancer and its clinical significance. Methods Immunohistochemical experiment was used to detect the expression of S100A16 protein in pancreatic cancer tissues and adjacent tissues, and we analyzed the relation between S100A16 positive expression and clinicopathological parameters, prognosis of pancreatic cancer patients. PPI was used to predict a protein relationship network that directly interacted with S100A16. Results The positive rate of S100A16 expression in cancer tissues was significantly higher than that in adjacent tissues (P=0.001). S100A16 expression was higher in patients with vascular infiltration and lymph node metastasis. The overall survival time of patients with pancreatic cancer was related to tumor size, TNM stage and S100A16 expression level. Multivariate analysis showed that the expression level of S100A16 was an independent risk factor for the prognosis of pancreatic cancer patients, and the risk of death in patients with high S100A16 expression increased by 1.5 times. PPI predicted that S100A16 and S100A14, IL36G, PITX1, PERP played an important role in the interaction network. Conclusion Pancreatic cancer patients with high S100A16 expression have poor prognosis. The positive expression of S100A16 is an independent prognostic indicator.
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Objective To investigate the synergistic effect of 11 β-hydroxysteriod dehydrogenase (11 β-HSD1) and S100A16 on the differentiation of3T3-L1 preadipocytes and its mechanism.Methods Lentiviral vectors PLJM1-11β-HSD1 and PLJM1-S100A16-GFP were respectively constructed and co-transfected into 3T3-L1 preadipocytes.The cell strains expressing 11 β-HSD1/S100A16 were screened with 2.5 μg/ml puromycin for two weeks.Western blot was employed to verify the lentiviral carrier transfection effects.The expressions of marker genes related to the adipocyte differentiation were detected by mean of realtime PCR.Oil red O staining was used to observe the lipid droplet accumulation and the content of triglyceride was measured after differentiation of preadipocytes.The effect of 11β-HSD1 and S100A16 on PPARγ promoter activity was detected by luciferase reporter gene.Results Compared with the empty vector group,the expressions of 11β-HSD1 and S100A16 protein in the lentivirus cotransfected 3T3-L1 cell strain were significantly higher.After 3T3-L1 cell strain co-expressing 1 1β-HSD1 and S100A16 was induced to differentiate for 8 days,the lipid droplets accumulation and triglyceride content were siginificantly increased,along with increased expressions of adipocyte differentiation marker genes such as PPARγ,CCAAT/enhancer binding protein α,lipoprotein lipase,fatty acid synthase,and adipocyte fatty acid-binding protein,in comparison with 11 β-HSD1 or S100A16 overexpression.The result of reporter gene indicated that 11 β-HSD1/ S100A16 enhanced PPARγ promoter activity.Conclusions 11β-HSD1 and S100A16 may jointly promote the differentiation of 3T3-L1 preadipocytes through a synergistic effect on PPARγexpression and play a critical role in the development of obesity.
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Objective To investigate the effect and mechanism of S100A16 in the course of 3T3-L1 preadipocytes differentiation.MethodsA recombinant virus vector overexpressing S100A16 ( PLJM1-S100A16-GFP) was constructed and transfected into 3T3-L1 preadipocytes.The expression of S100A16 in the course of 3T3-L1 preadipocytes differentiated into adipocytes was detected by Western blot.The lipid droplets were observed by oil-red O staining and triglycercide (TG) content was measured by the TG measure kit.Levels of adipogenesis-associated genes such as PPARγ,CCAAT/enhancer binding protein ( C/EBP-α),lipoprotein lipase ( LPL),fatty acid synthase ( FAS),adipocyte fatty acid binding protein( aP2 ) were measured by realtime PCR and Western blot.The interaction between S100A16 and p53 was detected by immunoprecipitation.Results3T3-L1 cell line overexpressing S100A16was successfully contructed.It was found that the expression of S100A16 was increased during 3T3-L1 adipocytes differentiation.Overexpression of S100A16 stimulated 3T3-L1 preadipocytes differentiation and increased the accumulation of triglycerides in adipocytes (P＜ 0.01 ),along with the up-regulation of adipocyte differentiationassociated gene expressions including PPARγ,C/EBP-α,LPL,aP2,and FAS ( P ＜ 0.05 or P ＜ 0.01 ).Immunoprecipitation analysis revealed that S100A16 interacted with tumor suppressor protein p53,also a known inhibitor of adipogenesis.ConclusionS100A16 stimulates 3T3-LI preadipocytes differentiation via inhibiting p53activity.