目的:分析45例胰腺癌及其配对癌旁正常石蜡包埋组织中mi R216a的表达情况,检测m i R216a的作用靶基因J A K2、C S K的蛋白表达水平,并分析mi R216a及JAK2、CSK蛋白表达水平与临床病理特征的关系,及其相关性.方法:锁定核酸原位杂交法测...目的:分析45例胰腺癌及其配对癌旁正常石蜡包埋组织中mi R216a的表达情况,检测m i R216a的作用靶基因J A K2、C S K的蛋白表达水平,并分析mi R216a及JAK2、CSK蛋白表达水平与临床病理特征的关系,及其相关性.方法:锁定核酸原位杂交法测定胰腺癌及癌旁正常组织中mi R216a的表达,免疫组织化学法测定JAK2、CSK蛋白的表达,并分析mi R-216a与JAK2、CSK之间的相关性,及其与胰腺癌临床病理指标的关系.结果:锁定核酸原位杂交法测定的mi R216a在胰腺癌组织中的阳性表达率为37.8%(17/45),癌旁正常组织的阳性表达率为71.1%(32/45),差异具有统计学意义(?2=10.080,P<0.05);免疫组织化学法测定胰腺癌组织中JAK2蛋白的阳性表达率为60%(27/45),癌旁正常组织为35.6%(16/45),差异具有统计学意义(?2=5.388,P<0.05);C S K在胰腺癌中的阳性表达率为17.8%(8/45),癌旁正常组织为73.3%(33/45),差异具有统计学意义(?2=27.999,P<0.05).mi R216a的表达水平与胰腺癌的TNM分期有关,而与患者年龄、性别、肿瘤分化程度,局部淋巴结转移、远处转移无关(P>0.05);JAK2、CSK的表达均与胰腺癌的分化程度有关,而与患者年龄、性别、TNM分期,局部淋巴结转移、远处转移无关(P>0.05).结论:mi R216a在胰腺癌组织中表达下调,JAK2在胰腺癌组织中表达上调,CSK在胰腺癌组织中表达下调,mi R216a可能通过靶向调节JAK2、CSK的表达,对胰腺癌的发病起到抑制作用.展开更多
AIM:To investigate the mechanisms by which Cskbinding protein(CBP)inhibits tumor progression in esophageal carcinoma.METHODS:A CBP overexpressing esophageal carcinoma cell line(TE-1)was established.The growth,invasion...AIM:To investigate the mechanisms by which Cskbinding protein(CBP)inhibits tumor progression in esophageal carcinoma.METHODS:A CBP overexpressing esophageal carcinoma cell line(TE-1)was established.The growth,invasion,and migration of CBP-TE-1 cells,as well as the expression of Src were then determined and compared with those in normal TE-1 cells.RESULTS:The expression of Src was decreased by the overexpression of CBP in TE-1 cells.The growth,invasion,and migration of TE-1 cells were decreased by the overexpression of CBP.CONCLUSION:This study indicates that CBP may decrease the metastasis of esophageal carcinoma by inhibiting the activation of Src.CBP may be a potential tumor suppressor and targeting the CBP gene may be an alternative strategy for the development of therapies for esophageal carcinoma.展开更多
文摘目的:分析45例胰腺癌及其配对癌旁正常石蜡包埋组织中mi R216a的表达情况,检测m i R216a的作用靶基因J A K2、C S K的蛋白表达水平,并分析mi R216a及JAK2、CSK蛋白表达水平与临床病理特征的关系,及其相关性.方法:锁定核酸原位杂交法测定胰腺癌及癌旁正常组织中mi R216a的表达,免疫组织化学法测定JAK2、CSK蛋白的表达,并分析mi R-216a与JAK2、CSK之间的相关性,及其与胰腺癌临床病理指标的关系.结果:锁定核酸原位杂交法测定的mi R216a在胰腺癌组织中的阳性表达率为37.8%(17/45),癌旁正常组织的阳性表达率为71.1%(32/45),差异具有统计学意义(?2=10.080,P<0.05);免疫组织化学法测定胰腺癌组织中JAK2蛋白的阳性表达率为60%(27/45),癌旁正常组织为35.6%(16/45),差异具有统计学意义(?2=5.388,P<0.05);C S K在胰腺癌中的阳性表达率为17.8%(8/45),癌旁正常组织为73.3%(33/45),差异具有统计学意义(?2=27.999,P<0.05).mi R216a的表达水平与胰腺癌的TNM分期有关,而与患者年龄、性别、肿瘤分化程度,局部淋巴结转移、远处转移无关(P>0.05);JAK2、CSK的表达均与胰腺癌的分化程度有关,而与患者年龄、性别、TNM分期,局部淋巴结转移、远处转移无关(P>0.05).结论:mi R216a在胰腺癌组织中表达下调,JAK2在胰腺癌组织中表达上调,CSK在胰腺癌组织中表达下调,mi R216a可能通过靶向调节JAK2、CSK的表达,对胰腺癌的发病起到抑制作用.
基金Supported by Gansu Provincial Natural Science Foundation,No.1308RJZA188the Fundamental Research Funds for the Central Universities,No.lzujbky-2011-T03-16
文摘AIM:To investigate the mechanisms by which Cskbinding protein(CBP)inhibits tumor progression in esophageal carcinoma.METHODS:A CBP overexpressing esophageal carcinoma cell line(TE-1)was established.The growth,invasion,and migration of CBP-TE-1 cells,as well as the expression of Src were then determined and compared with those in normal TE-1 cells.RESULTS:The expression of Src was decreased by the overexpression of CBP in TE-1 cells.The growth,invasion,and migration of TE-1 cells were decreased by the overexpression of CBP.CONCLUSION:This study indicates that CBP may decrease the metastasis of esophageal carcinoma by inhibiting the activation of Src.CBP may be a potential tumor suppressor and targeting the CBP gene may be an alternative strategy for the development of therapies for esophageal carcinoma.
