Objective To investigate the expression of phosphorylation-mammalian target of rapamycin (p-mTOR) in endometrial carcinoma. Methods The expressions of p-mTOR protein in tissues from 45 cases of endometrial adenocarcinoma, 7 endometrial atypical hyperplasia, and 6 normal endometrium were detected by immunohistochemistry SP method. Results The expression of p-mTOR protein maily restricted to cytoplasm. Compared with normal endometrium, the expression of p-mTOR protein in the cases of endometrial atypical hyperplasia and endometrial adenocarcinoma was significantly up-regulation(2.36 ± 0.76vs 6.21 ± 1.19, 15.82 ± 2.64)( F = 11.37, P ＜ 0.05 ). There was significant difference of p-mTOR protein in different histology class in endometrial adenocarcinoma (F = 8.27, P ＜ 0.05), but there was no significant difference of p-mTOR protein in different pathological grade in endometrial adenocarcinoma (P ＞0.05).Conclusion The expression of p-mTOR protein may participate in the occurrence and development of endometrial carcinoma.

Objective Long noncoding RNA (lncRNA) has been identified to regulate DNA methylation, histone acetylation, and gene post-transcriptional regulation in kinds of diseases, including tumorigenesis, obesity and so on.Therefore, lncRNAs might be the potential targets of mesangial cells proliferation.Methods Mesangial cells were exposed to suitable concentration of TGF-β through cell proliferation assay;then the lncRNAs expression levels were detected by microarray in experimental group and control group separately;finally the differentially expressed lncRNAs were identified by RT-PCR;meanwhile, and the expression levels of target genes were also detected by RT-PCR.Results Cell viability assay confirmed that 10 ng/ml TGF-β could promote mesangial cell proliferation significantly.Totally, over 30 000 lncRNAs were detected in TGF-β treated MCs and control group cells separately.Compared to the control group, 5550 lncRNAs differentially expressed in TGF-β treated MCs, including 119 up-regulated and 147 down-regulated over 2 fold.RT-PCR results appeared that uc.60, MRAK079149, MRAK029456, XR_005507, XR_007641, uc.14, and uc.412 were significantly up-regulated in TGF-β treated MCs, and BC088254, DQ402472, BC098733, BC158832,BC098746 were stably down-regulated.Compared to the control group, the mRNA expression levels of AATF and NEK were increased in the TGF-β treated mesangial cells (P ＜ 0.05).AATF and NEK were downstream target genes of uc.412 and MRAK079149 respectively.Conclusion The differential expression of long noncoding RNAs presents in the experimental mesangial cells proliferation induced by TGF-β.

Objective To investigate the effect of insulin (INS) on nuclear factor-kappa B (NF-KB) activation in glomerular mesangial cells(GMC) of the Zucker rats,and the correlation between the activity of NF-kB induced by insulin to the ages and genotype of Zucker rats. Methods (1) Four groups of cultured GMCs(O3m,O10m,L3m and L10m) from the Zucker obese rats(3 months old and 10 months old) and Zucker lean rats(3 months old and 10 months old) were stimulated by insulin. (2) Electrophoretic mobility shift assay (EMSA) was used to detect the activity of NF-KB. Gel supershift assay was used to detect the subunit of NF-KB dimer. (3) The protein of NF-KB p65 in cytoplasm and cytoblast was analysed by Western Blot. Results (1) NF-KB activity in 4 groups GMCs was significantly higher than that in control group after induced of INS ( F=219. 65 P

Aim Tostudythetherapeuticeffectof CJ016 on human lung cancer model and the mecha-nism.Methods Anexperimentalhumanlungadeno-carcinoma model of A549 was set up to investigate the anti-tumor effect of CJ016,while the effect of angio-genesis and apoptosis in tumor were detected.Results In vitro,the cell proliferation was inhibited signifi-cantly by CJ016,and the value of IC50 was 34. 22 nmol ·L-1 .In vivo,the tumor inhibition rate and T/C%value were 70. 08%and 27. 75%,respectively,at the dose of 20 mg·kg-1 .Meanwhile,CJ016 could reduce the expression of CD31 and promote the apoptosis of tumorcells.Conclusion CJ016caninhibitthegrowth of A549 cells,and the possible mechanism may be re-lated to the reduction of angiogenesis and inducing tumor cell apoptosis.

Objective To investigate the role of vitamin D receptor (VDR) in the protection of bufalin on podocyte injury induced by adriamycin (ADR).Methods (1) In vitro:the toxic effect of different concentrations of bufalin (10-9,10-8,10-7,104 mol/L) on podocyte was evaluated by lactate dehydrogenase (LDH) test;Annexin V-FITC and RT-PCR were utilized for podocyte apoptosis and VDR mRNA level respectively.Western blotting was used to analyze the protein expression of VDR and nephrin.SiRNA intervene was also applied to evaluate the role of VDR in bufalin's protective effect on podocyte injury induced by ADR.(2) In vitro:24 SD rats were randomly divided into three groups:control group,ADR group and ADR+bufalin group.TUNEL assay was applied to detect the apoptosis of podocytes in the kidney.Immunofluorescence and transmission electron microscope (TEM) were applied to analyze the expression of VDR and the ultrastructure of the glomerulus.Results Bufalin concentration lower than 10-7 mol/L had no toxicity on normal podocyte.Bufalin reduced the urinary protein excretion (P ＜ 0.05),alleviated the removal of podocyte foot processes and attenuated the changes in nephrin expression in the glomerulus of the adriamycin (ADR) rats (P ＜ 0.05).Bufalin notably inhibited the down-regulation of VDR in protein levels on the glomerulus of the ADR rats.Additionally,bufalin inhibited the down-regulation of VDR in both mRNA levels and protein levels (P ＜ 0.05),nephrin protein expression (P＜ 0.05),and apoptosis induced by ADR in cultured podocytes.Additionally,VDR specific siRNA intervene abolished the protective effect of bufalin in ADR-induced podocyte injury.Conclusion Bufalin can alleviate ADR-induced podocyte injury via enhancing VDR expression.

Objective To study the clinical significances of CD14bright CD16bright cell subset in pe-ripheral blood of patients with gastric cancer (GC). Methods The CD14bright CD16bright cells in peripheral blood samples collected from 124 patients with gastric cancer ( GC), 130 patients with chronic gastritis (CG) and 80 normal healthy controls (HC) were measured by using flow cytometry. Differences in the CD14bright CD16bright cells between different groups were analyzed with the Mann-Whitney U test. The feasibili-ty of using CD14bright CD16bright cells as a potential biomarker for differentiating GC patients from CG was as-sessed by using the receiver operating characteristic ( ROC) curve analysis. Correlations between the CD14bright CD16bright cells and clinicopathologic parameters of GC were analyzed with multivariate correlation analysis. Results The percentages of CD14bright CD16bright cells in peripheral blood samples and in CD14bright monomuclear cells collected from the patients with GC [median: 0. 38% (0. 23% -0. 52% ) and 6. 61%(4. 23% -9. 56% )] were significantly higher than those of the CG and HC groups [ median: 0. 11%(0. 07% -0. 15% ) and 5. 08% (3. 35% -6. 42% ); median: 0. 05% (0. 03% -0. 07% ) and 5. 09%(4. 20% -7. 40% )] (P<0. 01). The area under the ROC curve for CD14bright CD16bright cells in the peripher-al blood was 0. 934 (95% CI: 0. 900-0. 968) indicating that the value of CD14bright CD16bright cells in the di-agnosis of GC was much higher than that of alpha fetoprotein (AFP), cacino-embryonic antigen (CEA) and carbohydrate antigen CA199. The area under the ROC curve for combined multi-markers by using logistic model (CD14bright CD16bright cell subset and serum tumor markers) was 0. 947 (95% CI: 0. 920-0. 973). The CD14bright CD16bright cells were closely associated with lymphocyte cells ( P < 0. 01). Conclusion The CD14bright CD16bright cells were dramatically increased in the peripheral blood of patients with gastric cancer, which could be used as a biomarker in the diagnosis of gastric cancer.

Objective To study the correlation between human leucocyte antigen-G (HLA-G) 14 bp insertion/deletion (I/D) polymorphism and susceptibility to non-small cell lung cancer (NSCLC) as well as poor prognosis in NSCLC.Methods A total of 113 patients with NSCLC and 150 age-and sex-matched healthy subjects were genotyped by PCR to analyze the HLA-G 14 bp insertion/deletion polymorphism in them.Epidermal growth factor receptor (EGFR) gene mutation in patients with NSCLC was detected by using amplification refractory mutation system (AMRS).Expression of HLA-G in NSCLC tissues was detected with immunohistochemistry.All patients with NSCLS were followed up to collect survival data, which were further analyzed with Kaplan-Meier method.Results The frequency of HLA-G 14 bp D/D genotype was significantly higher in the patients with NSCLC than that in the healthy subjects (x2=3.907, P=0.048, OR=1.66).Among the patients with NSCLC, HLA-G 14 bp I/I genotype carriers had a shorter overall survival time as compared with that of HLA-G 14 bp I/D or HLA-G 14 bp D/D genotype carriers (P=0.005).Patients who received chemotherapy or radiation had significantly shorter survival time than those received EGFR-targeted therapy (P=0.001).Among patients who were positive for EGFR mutation, HLA-G 14 bp D/D genotype carriers had longer survival time than those carrying HLA-G 14 bp I/I or HLA-G 14 bp I/D genotype (P=0.041).The expression of HLA-G was closely correlated with HLA-G 14 bp polymorphism in patients with NSCLC (P=0.001).Conclusion These data, reported for the first time, indicates that HLA-G 14 bp polymorphism might be a genetic factor related to the susceptibility to NSCLC and associated with survival in patient with NSCLC after excluding the interference of molecular targeted agents.

Purpose:To investigate the main prognostic factors of patients with renal cell carcinoma.Methods:104 cases of patients with postoperative renal cell carcinoma were analyzed by Cox regression models.Results:Four factors showed significant relation to prognosis: clinical stage, radical nephrectomy for renal cell carcinoma, hematuria, embolization of renal artery. A predicting equation was established, and the predicting values were calculated according to the individual features of patients. The predicting and actual values were compared, and the sensitivity, specificity and overall concordance were 73.3%, 83.3%, and 80.4% respectively.Conclusions:Radical nephrectomy for renal cell carcinoma and embolization of renal artery were protective factors of renal cell carcinoma and the clinical stage and hematuria were risky factors.

Objective To evaluate the therapeutic effect of microwave ablation in combination with TACE for the treatment of primary liver carcinoma (PLC). Methods From Jan. 2004 to Dec. 2008, 63 PLC patients underwent ultrasound-guided microwave ablation (percutaneous or open) under general anesthesia. Repeated microwave ablation or TACE was used when an incompleted ablation or recurrence was found during postoperative regular follow-up. Results These 63 PLC patients have received a total of 82 sessions of microwave ablation procedure (1 to 5 sessions for each patient). There were 2 early postoperative deaths with a procedure-related mortality of 3.2%. At the end of the follow-up, 22 patients were alive and 38 died,and the other one was lost to follow-up. The survival rates in 1,2 and 3 years were 63.3%,42.1% and 26.5%, respectively, with a median survival of 20 months for all patients. The survival for PLC patients with early stage (TNM Ⅰ and Ⅱ) was significantly longer than that of advanced stage (TNM Ⅲ and Ⅳ). The 1,2 and 3 year's cumulative survival rate was 93.3%,86.7% and 65.0% respectively in those 15 cases with only single tumor and the diameter≤3 cm, which were significantly longer than that of other PLC patients. Of 23 patients with recurrence,9 had solitary tumor without lymphnode and distal metastases, for which the survival rates in 1,2 and 3 years were 100%,88.9%, and 35.6%, respectively, whereas in other recurrent patients the survival rates in 1,2 and 3 years were 21.4%, 10.7% and 0%, respectively(P< 0.01). Conclusions Ultrasound-guided microwave ablation in combination with TACE is effective for PLC patients with early stage. In recurrent PLC patients after ablation therapy with solitary tumor and no lymphnode and distal metastases the survival is significantly longer than that of the others.

Objective To investigate the roles of human leukocyte antigen-G ( HLA-G) in mye-loid-derived suppressor cell (MDSC) proliferation and M1/M2 macrophage differentiation in C57BL/6-NCI-H446-G tumor-bearing mice for better understanding the mechanisms of HLA-G involved in tumor immune evasion. Methods NCI-H446 ( human small cell lung cancer cells) and NCI-H446-G ( NCI-H446 cells ex-pressing HLA-G) cells were labeled with CFSE at a final concentration of 1μmol/L. CFSE fluorescence lev-els were measured by flow cytometry at different time points. Mouse tumor models were established by subcu-taneous injection of C57BL/6 mice with NCI-H446 and NCI-H446-G cells, respectively. PBS was used to set up negative control group. The mice in each group were sacrificed to collect tissue samples on 5 d, 10 d, 15 d and 20 d after injection. The percentages of splenic CD11b+Gr1+MDSCs, F4/80+CD80+M1 and F4/80+CD206+M2 macrophages were analyzed by flow cytometry. Results Steady expression of HLA-G in NCI-H446-G cells was confirmed by Western blot and flow cytometry. HLA-G enhanced the proliferation of NCI-H446 cells. Tumor size increased dramatically in tumor-bearing mice in the first five days and then de-creased over time. The tumor-bearing mice in the NCI-H446-G group had larger tumor than those in the NCI-H446 group in every time point (P<0. 05) and required longer time to fully reject the tumor. Compared with the PBS and NCI-H446 groups, the percentage of splenic MDSCs in tumor-bearing mice was significantly in-creased in the NCI-H446-G group (P<0. 05). Moreover, the ratio of M1/M2 in NCI-H446-G tumor-bearing mice was much lower than that in the other two groups (P<0. 05). Conclusion This study indicated that HLA-G could increase the percentage of MDSCs and decrease the ratio of M1/M2, which might illustrate the role of HLA-G in tumor immune evasion and its potential clinical significance in cancer immunotherapy.