机构地区:[1]蚌埠医学院第一附属医院病理科,安徽蚌埠233003 [2]南京医科大学动脉粥样硬化研究中心,南京210029
出 处:《临床检验杂志》2014年第3期196-199,共4页Chinese Journal of Clinical Laboratory Science
基 金:安徽省自然科学基金项目(1208085MH152);安徽省高等学校省级优秀青年人才基金项目(2012SQRL096);蚌埠医学院科技发展基金项目(Bykf12B17)
摘 要:目的探讨子宫内膜样腺癌中垂体瘤转化基因1(PTTG1)、抑癌基因1(BRCA1)和血管内皮生长因子(VEGF)基因的表达和意义。方法用western blot检测138例子宫内膜样腺癌、32例子宫内膜不典型增生、40例正常子宫内膜组织中PTTG1、BRCA1和VEGF蛋白的表达水平;用实时荧光定量PCR检测上述组织中PTTG1、BRCA1和VEGF mRNA表达水平;分析3个指标的相关性及与患者5年生存率的关系;western blot检测子宫内膜样腺癌中PTTG1相关的信号通路Akt和STAT3蛋白的激活情况。结果 PTTG1、VEGF mRNA在子宫内膜癌中的表达量为5.44±1.04、3.62±0.78,在不典型增生内膜组织中的表达量为3.24±0.72、2.32±0.73,在正常内膜组织中的表达量为1.65±0.40、1.02±0.25,差异均有统计学意义(P<0.01);PTTG1、VEGF蛋白在子宫内膜癌中的表达量为1.23±0.14、1.57±0.24,在不典型增生内膜组织中的表达量为0.89±0.13、0.86±0.08,在正常内膜组织中的表达量为0.54±0.10、0.42±0.06,差异均有统计学意义(P均<0.05);而BRCA1 mRNA和蛋白质在3种组织中表达差异无统计学意义(P>0.05)。子宫内膜样腺癌组织中PTTG1与VEGF的表达呈正相关(r=0.385,P<0.01),与BRCA1的表达无相关关系(r=0.028,P>0.05)。与正常内膜组织相比,子宫内膜样腺癌组织中Akt、STAT3可被磷酸化激活(P均<0.05)。结论子宫内膜样腺癌患者PTTG1过度表达可伴随VEGF表达上调及p-Akt和pSTAT3的激活,推测PTTG1可能参与子宫内膜样腺癌的发生、发展。Objective To investigate the expression and significance of pituitary tumor-transforming gene 1 (PTTG1), breast cancer gene 1 (BRCA1)and vascular endothelial growth factor (VEGF) gene in endometrioid adenoeareinoma. Methods The protein levels of P^G1, BRCA1 and VEGF in 138 endometrioid adenoeareinoma, 32 atypical hyperplasia and 40 normal endometrial tissue samples were evaluated by western blot and the mRNA levels of PTTG1, BRCA1 and VEGF were identified by real-time PCR. The correlation a- mong the three parameters and the relationship of the parameters with the prognosis of patients was analyzed. The activations of Akt and STAT3 of PTTGl-associated signaling pathway proteins in the samples of endometrioid adenocarcinoma were detected by western blot. Results The mRNA expression levels of PTTG1 and VEGF were ( 5.44 _± 1.04 ) and ( 3.62 ± 0. 78 ) in endometrioid carcinoma; ( 3.24 ± 0. 72 ) and (2.32 ± 0.73 ) in atypical hyperplasia, and ( 1.65 ± 0.40 ) and ( 1.02 ± 0.25 ) in normal endometrium ( P 〈 0.01 ). The protein levels of PTTG1 and VEGF were (1.23 ± 0.14) and (1.57 ± 0.24 ) in endometrioid adenocarcinoma, (0.89 ± 0.13 ) and (0.86 ± 0.08 ) in atypical hyperplasia, and (0.54 ± 0.10) and (0.42 ± 0.06) in normal endometrium ( P 〈 0.05 ). No difference of the mRNA or protein expression levels of BRCA1 was found among the samples of normal endometrium, atypical hyperpla- sia and endometrioid carcinoma. Statistical analysis showed a positive correlation of VIq'G1 with VEGF in endometrioid carcinoma ( r = 0. 385, P 〈 0.01 ), but no correlation between P'Iq'G1 and BRCA1 (r = 0. 028, P 〉 0.05 ). Akt and STAT3 were activated by phos- phorylation in endometrioid adenoearcinoma tissue compared with normal endometrioid tissue ( P 〈 0.05 ). Conclusion The overex- pression of PTTG1 in the patients with endometrioid adenocarcinoma may upregulate the expression of VEGF and activate p-Akt and p- STAT3 pathways, which
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