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Objective To investigate the expression and significance of cellular inhibitor of protein phosphatase 2A (CIP2A), bcl-2 and p63 in papillary thyroid cancer (PTC). Methods Using immunohistochemistry to detect the expression of CIP2A, bcl-2 and p63 in 30 cases of nodular goiter (NG), 30 cases of thyroid adenoma (TA) and 57 cases of PTC [including classical PTC (cPTC) 20 cases, papillary microcarcinoma (PMC) 20 cases, follicular thyroid papillary carcinoma (FPTC) 7 cases]. Results In NG group, TA group and PTC group, positive rates of CIP2A were 0, 0 and 94.74 % (54/57), respectively. The differences were statistically significant. In NG group, TA group and PTC group, positive rates of bcl-2 were 16.67 % (5/30), 13.33 % (4/30) and 85.96 % (49/57), respectively. The differences were statistically significant. In each group, positive rates of p63 were 6.67% (2/30), 3.33% (1/30) and 5.26% (3/57), respectively, no significant difference among them. In PTC, expression of CIP2A and bcl-2 were significantly higher than in NG and TA (χ2 = 105.56, P= 0.00; χ2 = 58.95, P= 0.00). Furthermore, the expression of CIP2A and bcl-2 had correlation in PTC (r=0.94, P=0.00). The expression of CIP2A, bcl-2 and p63 had no significantly difference among all the PTC subtype (χ2 values were 2.02, 2.64, 1.85; all P> 0.05). The expression of CIP2A, bcl-2 and p63 was not associated with patients'age, sex, site, lymph node metastasis (all P>0.05). Conclusions High expression of CIP2A and bcl-2 is associated with PTC, and the expression of CIP2A and bcl-2 has correlation in PTC. The expression of p63 has no correlation with PTC.
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Objective To investigate the effect of flavopiridol on the proliferation,invasiveness and apoptosis of human prostate cancer cell line LNCaP,and to explore the possibility of its application in clinical treatment.Methods MTT assay was used to detect cell proliferation,cell invasion in vitro was detected by Transwell assay,and flow cytometer was used to observe apoptosis.Results Flavopiridol inhibited the growth of LNCaP cells in a concentration-dependent and time-dependent way (P ＜ 0.05),and reduced the ability of invasion capacity.After treated by 10 nmol/L flavopiridol for 24 h,the apoptosis rate was increased significantly to (7.5±0.9) ％ compared with the control group [(5.3±0.5) ％] (P ＜ 0.05).Conclusion Flavopiridol can inhibit proliferation of LNCaP cells and induce apoptosis,which may be applicable for the treatment of prostate cancer.
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Objective To investigate the effect of histone deacetylase inhibitor trichostatin A (TSA) on the chemotherapy sensibility of 5-fluorouracil (5-Fu) in colorectal cancer cell line Lovo, and to explore the possible mechanisms.Methods According to the treatment methods, the cells were divided into control group, 5-Fu group, TSA group, TSA preconditioning group and combination group (TSA+5-Fu).MTT assay was used to detect cell proliferation at 24 h, 48 h and 72 h after drugs treatment.Transwell assay was used to test cell invasion after 24 h drugs treatment.Flow cytometer was applied to observe the apoptosis after 24 h drugs treatment.The expressions of thymidylate synthase (TS) were detected by Western blot after 24 h drugs treatment.Results Compared with control group, the 5-Fu group, TSA preconditioning group and combination group had a growth inhibition to Lovo cell at 24 h, 48 h and 72 h (P ＜ 0.05), and compared with 5-Fu group, the growth inhibition of TSA preconditioning group and combination group were distinctive at 48 h and 72 h (P ＜ 0.05).However, the inhibition between TSA preconditioning group and combination group were no significant (P ＞ 0.05).Interfered after 24 h, the number of cells penetrating the matrigel in control group, 5-Fu group, TSA group,TSA preconditioning group and combination group were (25.0±4.2), (16.8±2.8), (19.6± 2.5), (8.2±3.2) and (6.5±2.6), respectively (P ＜ 0.05), and the apoptosis rates were (4.26±1.36) ％, (11.66± 3.18) ％, (8.57±2.69) ％, (39.79±8.53) ％ and (45.18±10.07) ％, respectively (P ＜ 0.05).Compared with control group, the number of cells penetrating the matrigel in the experimental groups was significantly decreased, and the apoptosis rate was significantly increased (P ＜ 0.05).Compared with 5-Fu group, the numbers of cells penetrating the matrigel in TSA preconditioning group and combination group were markedly decreased, and the apoptosis rates were markedly increased (P ＜ 0.05), but the number of cells penetrating the matrigel and the apoptosis rate between TSA preconditioning group and combination group were not different (P ＞ 0.05).The difference of TS expression between control group and 5-Fu group was not significant (P ＞ 0.05).Compared with that in control group and 5-Fu group, TS expressions in TSA group, TSA preconditioning group and combination group were markedly decreased (P ＜ 0.05), but TS expressions among the last three groups were not different (P ＞ 0.05).Conclusion TSA can increase the chemotherapy sensibility of 5-Fu in Lovo cells, which may be dependent on reducing the TS expression.
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Objective To investigate the effect of shRNA-mediated down-regulation of the receptor for activated C kinase 1 (RACK1) gene on the chemotherapeutic sensitivities in human lung adenocarcinoma cell line A549.Methods The shRNA recombinant plasmid targeting to human RACK1 gene was designed and transferred into A549 cells by lipofectin technique.The protein level of RACK1 was measured by Western blot to confirm the function of shRNA plasmid.Drug sensitivities of A549 cells to cisplatin,gemcitabine,pemetrexed and paclitaxel were analyzed by MTT assay.The protein expression of LRP and MRP were detected by Western blot.Results After 24 hours transfection,the relative expression quantity of RACK1 protein in RACK1-shRNA group was 0.267± 0.470,which was significantly lower than that in vector-shRNA group (0.821±0.109) and control group (0.842±0.060) (F =54.438,P ＜ 0.05).The results of MTT showed that the growth of A549 cells in the RACK1-shRNA group was markedly inhibited.The sensitivities of A549 cells to cisplatin and paclitaxel were significantly enhanced compared with that in the vector-shRNA group and control group (P ＜ 0.05).The relative expression quantity of LRP and MRP protein in RACK1-shRNA group were 0.163±0.056 and 0.246±0.050,which were lower than that in vector-shRNA group and control group (F LRP =19.430,F MRP =61.548,both P ＜ 0.05).Conclusion Targeted gene silencing of RACK1 improves the sensitivity of A549 cells to the ascisplatin and paclitaxel medicines,which might be achieved through down-regulation of the expression of LRP and MRP.
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BACKGROUND:In recent years, the effectiveness of stem cel transplantation in the treatment of spinal cord injury has been validated in animal models, and mesenchymal stem cel transplantation for treatment of spinal cord injury has been studied most widely. Currently, there are a number of relevant clinical studies that have shown a good prospect. OBJECTIVE:To evaluate the efficacy and safety of mesenchymal stem cel transplantation for spinal cord injury in human with a system review. METHODS:PubMed database, EMBASE database, Cochrane Library, ISI Web of knowledge, CBM database, VIP database, CNKI database and Wanfang database were searched from their start year up to July 2015 for relevant randomized clinical trials on the treatment of spinal cord injury with mesenchymal stem cel transplantation. The key words were“spinal cord injury, paraplegia, cel transplantation, transplantation, mesenchymal stem cel , bone marrow transplantation, stem cel , randomized control ed trial”in English and Chinese, respectively. RESULTS AND CONCLUSION:A total of 260 articles were retrieved, including 6 randomized clinical trials (252 cases). In the aspects of ASIA touch sensation score, overal Frankel score and daily life activity training score, the patients undergoing mesenchymal stem cel transplantation were significantly superior to those in the control group (P0.05). Compared with the control group, low fever was more common in the patients undergoing mesechymal stem cel transplantation (P0.05). These findings suggest that mesenchymal stem cel transplantation has limited efficacy in the treatment of spinal cord injury and cannot induce severe complications, but there is a need for high-quality randomized control ed trials to prove the efficiency and safety of mesenchymal stem cel transplantation for the treatment of spinal cord injury.
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Objective To investigate the expression of the enhancer of zeste homolog 2 (EZH2) gene and its significance in colorectal adenocarcinoma.Methods Immunohistochemistry and Western blot was used to assess the expression of EZH2 in human colorectal adenocarcinoma tissues,colorectal adenoma tissues and non-cancerous adjacent colorectal tissues.The relationships between EZH2 and each clinical pathology parameter were analyzed.Results The results of immunohistochemical trail showed that the expression rates of EZH2 in colorectal adenocarcinoma,colorectal adenoma and non-cancerous adjacent colorectal tissues were 80.56 ％ (87/108),62.5 ％ (25/40) and 5.00 ％ (2/40),respectively (P ＜ 0.05).Western blot revealed that the expression level of EZH2 in colorectal adenocarcinoma tissues,colorectal adenoma tissues and non-cancerous adjacent colorectal tissues level 0.549±0.145,0.283±0.023 and 0.107±0.022,respectively.The level in colorectal adenocarcinoma tissues (0.549±0.145) and colorectal adenoma (0.283±0.023) was significantly higher than that in non-cancerous adjacent colorectal tissues (0.107±0.022).Compared with colorectal adenoma tissues,level in colorectal adenocarcinoma tissues was significantly higher.There were significant differences among the three groups (F =20.113,P ＜ 0.05).The ratio of high expression level of EZH2 in colorectal adenocarcinoma tissues was closed related with tumorgenesis,differentiation,TNM staging and lymphatic metastsis (all P ＜ 0.05).However,no correlation was revealed between EZH2 expression and the age,gender (both P ＞ 0.05).Conclusion The expression of EZH2 may be associated with the tumorgenesis invasion,metastasis and progression of colorectal adenocarcinoma.
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Objective To investigate the expression of protein interacting with Cα kinase 1 (PICK1) and its significance in colorectal adenocarcinoma.Methods The expression of PICK1 were detected by immunohistochemistry and Western blot methods in tissues of colorectal adenocarcinoma,colorectal adenoma,colorectal polyp and adjacent tissues.The correlation between PICK1 and clinical pathological data was explored.Results Immunohistochemical assay showed that the positive ratio of PICK1 protein was 72.5 ％ (74/102),and overexpressed in 31 cases (30.4 ％,31/102) with colorectal adenocarcinoma.The ratio of high expression level of PICK1 in colorectal adenoma tissues (22.2 ％,8/36) was significantly higher than that in the adjacent tissues (0,0/40) (P ＜ 0.05).The ratio of high expression level of PICK1 in colorectal polyp tissues (5.6 ％,2/36) was no statistically difference compared with that of the adjacent tissues (P ＞ 0.05).Western blot analysis revealed that the expression of PICK1 in colorectal adenocarcinoma (1.10±0.04) was significantly higher than that in the adjacent tissues (0.75±0.07) (P ＜ 0.05).The result showed significant correlation with the tumor location,the degree of differentiation,depth of invasion,TNM stages and lymph metastasis (all P ＜ 0.05).However,there is no correlation was revealed between PICK1 expression and the patients age,gender (both P ＞ 0.05).Conclusion The expression of PICK1 may be associated with the tumorgenesis,progression,invasion and metastasis of colorectal adenocarcinoma,which contributes to the prognosis of patients.
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Objective To investigate the expression of Dysadherin and analyze its role in renal clear cell carcinoma (RCCC).Methods RT-PCR and immunohistochemical were used to detect the expression of Dysadherin in 60 cases of fresh RCCC and 60 adjacent normal renal tissues(male 35,female 25; age 37-78,median age 61; ＞7 cm 24,≤7 cm 36; Ⅰ/Ⅱ 39,Ⅲ/Ⅳ 21).Results Dysadherin mRNA expression in RCCC tissues (2.0043±0.2890) was higher than that in adjacent normal renal tissues (0.8461 ±0.2479) (t =6.8020,P ＜ 0.05).Dysadherin expression was associated with nuclear grade.The expression of Dysadherin in nucleus grade Ⅲ and Ⅳ tumors were significantly higher than that in nucleus grade Ⅰ and Ⅱ tumors [the mRNA expression were 4.6224±0.3194,2.7780±0.2288,the positive rates of protein were 64.1％ (25/39),95.2 ％ (20/21) (t =6.5750,x2 =5.495,P ＜ 0.05)].There was no association between the expression of Dysadherin with sex (t =1.0530,x2 =0.023),age(t =0.0511,x2 =0.089) and tumor size (t =1.0330,x2 =0.370) (P ＞ 0.05).Conclusion In RCCC,Dysadherin expression is positively associated with tumor aggressiveness based on grading.It seems that Dysadherin may be a valuable prognostic marker in RCCC.
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Objective To evaluate the association of c-erbB-2 protein expression with the prognosis of gastric carcinoma. Methods Eleven literatures were analyzed which published in recent 15 years on the relationship of c-erbB-2 with prognosis quantitively by software RevMan. Results The pooled odds ratio(OR) of 5-year survival rates was 0.69(95% CI:0.54～0.87)for all 11 literatures. The pooled odds ratio(OR) of three literatures from eleven literatures was 0.67(95%CI:0.48～0.94)which 5-year survival rates was determined as final index and OR as associated.For well-differentiated and advanced gastric carcinoma, the pooled odds ratio(OR) of 5～year survival rates were 0.18(95%CI:0.09～0.38)and 0.72(95%CI:0.47～1.09)respectively.Conclusion The association of c-erbB-2 expression with prognosis of gastric carcinoma is negative.
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AIM:To investigate the protective effect of losartan(Los) on apoptosis of H9c2 cells induced by isoprenaline(ISO),and to discover its related mechanism.METHODS:H9c2 cells cultured on plastic plates were divided into control,ISO,ISO+Los,ISO+Los+LY294002 and DMSO groups.Cell apoptosis was evaluated by flow cytometery and agarose gel electrophoresis.The mRNA levels of bax,bcl-2 and caspase-9 were detected by RT-PCR and the expressions of phosphorylated and total Akt(p-Akt and t-Akt) were assessed by Western blotting.The cAMP was measured by radioimmunoassay.RESULTS:ISO at concentration of 10 ?mol/L induced apoptosis of H9c2 with an increase in bax/bcl-2,caspase-9 and cAMP.Addition of 10 ?mol/L losartan inhibited apoptosis obviously with a decrease in bax/bcl-2,caspase-9 and cAMP.A significant increase in p-Akt was observed,and its protein level was elevated.LY294002 at concentration of 1 ?mol/L abolished the protective effects of losartan on ISO-induced apoptosis in H9c2 cells.CONCLUSION:ISO might induce H9c2 cell apoptosis through stimulation of ?-adrenergic receptor(?-AR).Los inhibits downstream signaling of ?-AR,and promotes the activation of Akt.Subsequently it might attenuate the apoptosis induced by ?-adrenergic stimulation of ISO.