Expression Of SIRT1 In Endometrial Carcinoma And Clinical Significance Of Its Expression In T2DM Patients

SIRTl is dependent on nicotinamide adenine dinucleotide(NAD) histone deacetylase which has got more attention. SIRT1 was originally considered to be a potential tumor promoter since it negatively regulates the tumor suppressor p53 and other tumor suppressors. There is new evidence that SIRT1 acts as a tumor suppressor based on its role in negatively regulating Survivin.Now there is less study of SIRT1 in EC, so it is important for anlysing the functions of SIRT1 in EC and its association with p53 and Survivin.SIRT1 took effect in tumorigenesis by many way,meanwhile it promoted insulin secretion and improved insulin resistance. There is growing evidence of a positive relationship between type 2 diabetes mellitus (T2DM) and cancer. Obesity, hypertension and Diabetes mellitus called EC triad.Nowardays there is less research for EC with T2DM of molecular biomarker expression but more clinical study. Anlysing the effect of blood glucose for SIRT1 by studying different expression of SIRT1 in endometrium with or without T2DM and association of SIRT1 and p53 or Survivin had correlation with SIRT1 in EC, Then anlyse the expression of SIRT1 in EC with T2DM and obtain evidence of prevention and cure, diagnosis and prognosis for EC of T2DM patients.Objective:To study the effect of SIRT1 in EC tumorigenesis and its correlation with p53 and Survivin.And the effect of blood glucose for SIRT1 in endometrium. Anlyse the expression and clinical significance of SIRT1 in EC with T2DM and association between SIRT1 and p53 or Survivin had correlate with SIRT1 in EC.Then obtain evidence of prevention and cure, diagnosis and prognosis for EC of T2DM patients.Method:Immunohistochemistry was carried out to examine the expression of SIRT1 in 39 cases of EC with T2DM,40 cases of EC,12 cases of normal endometrium with T2DM and 40 cases of normal endometrium.Investigated the expression of SIRT1 combining clinicopathologic features of EC and its correlation with p53 and Survivin. Anlyse the effect of blood glucose for SIRT1 by detecting different expression of SIRT1 in endometrium with or without T2DM.And then anlyse correlation between SIRT1 and p53 or Survivin correlate with SIRT1 in EC.Result:1 Expression of SIRT1 and its correlation with p53 and Survivinin ECExpression of SIRT1 was significantly increased in endometrial carcinoma tissues compared to normal endometrium (?2=36.473, P< 0.001).The expression of SIRT1 was closely associated with clinical stage and histological grade(P<0.05).Expression of p53 and Survivin was significantly increased in endometrial carcinoma tissues compared to normal endometrium(P<0.05).Expression of SIRT1 was positively correlated with p53 in EC(r=0.364, P=0.021).2 Effect of SIRT1 in regulating blood glucose and p53 in ECExpression of SIRT1 in endometrium with T2DM was lower than in endometrium (x 2= 1.000, P=0.752); Expression of SIRT1 was significantly decreased in endometrial carcinoma with T2DM compared to EC. (?2=4.561, P=0.033).There was no difference of expression of p53 between endometrial carcinoma with T2DM and EC.3 Expression of SIRT1 in EC with T2DM and its correlation with p53Expression of SIRT1 was significantly increased in endometrial carcinoma with T2DM compared to endometrium with T2DM (?2=11.421, P=0.001). The expression of SIRT1 was closely associated with clinical stage and histological grade(P<0.05).Expression of SIRT1 was positively correlated with p53 in EC with T2DM (r=0.360, P=0.024)Conclusions:1 SIRT1 is the promoter of EC. SIRT1, p53 and Survivin may take part in tumorigenesis and proliferation of EC. SIRT1 is an EC malignant and prognostic indicator. It is helpful for evaluating prognosis and clinical therapy to observe SIRT1 combined p53.2 Hyperglycosemia has no effect for SIRT1 in normal endometrium. Underlaying neoplasia,hyperglycosemia down-regulate SIRT1.Antineoplaston targeted SIRT1 may make insulin sensitivity more serious.3 The hyperexpession of SIRT1 in patients with DM means high risk to EC.We can evaluate EC with T2DM by SIRT1 as a malignant and prognostic indicator. It is more important for clinical significance to observe SIRT1 combined p53. Hyperexpession therapy escaping the effect of SIRT1 may decrease incidence rate of EC. Targeting SIRT1 antineoplaston may make insulin sensitivity more serious.Using activator of SIRT1 may increase malignant level.