目的探讨细胞S相激酶相关蛋白(S-phasekinase associated protein 2,Skp2)、p27蛋白与喉鳞状细胞癌(简称喉癌)各临床因素及预后的相关性。方法采用免疫组化SP法检测79例喉癌患者肿瘤组织的Skp2、p27表达。结果喉癌中Skp2高表达率(53.16%...目的探讨细胞S相激酶相关蛋白(S-phasekinase associated protein 2,Skp2)、p27蛋白与喉鳞状细胞癌(简称喉癌)各临床因素及预后的相关性。方法采用免疫组化SP法检测79例喉癌患者肿瘤组织的Skp2、p27表达。结果喉癌中Skp2高表达率(53.16%)显著高于正常喉组织(0%,P<0.05);喉癌Skp2蛋白低表达组的5年生存率(72.18%)显著高于高表达组(44.17%,P<0.01)。p27蛋白在喉癌和癌旁喉组织中的高表达率分别为30.38%和90%,差异具有显著性(P<0.05);喉癌p27蛋白高表达组的5年生存率(72.98%)显著高于低表达组(51.13%,P<0.01)。将Skp2和p27结合分析,Skp2高表达并p27低表达组的5年生存率最低,与另一组相比具有显著性差异(P=0.001)。结论Skp2蛋白通过降解靶蛋白p27可能在喉癌发生、发展中发挥重要作用。展开更多
AIM: To investigate the functional significance of insulin-like growth factor binding protein-5 (IGFBP-5) overexpression in pancreatic cancer (PaC).METHODS: The effects of IGFBP-5 on cell growth were assessed by stabl...AIM: To investigate the functional significance of insulin-like growth factor binding protein-5 (IGFBP-5) overexpression in pancreatic cancer (PaC).METHODS: The effects of IGFBP-5 on cell growth were assessed by stable transfection of BxPC-3 and PANC-1 cell lines and measuring cell number and DNA synthesis. Alterations in the cell cycle were assessed by flow cytometry and immunoblot analyses. Changes in cell survival and signal transduction were evaluated after mitogen activated protein kinase and phosphatidylinositol 3-kinase (PI3K) inhibitor treatment.RESULTS: After serum deprivation, IGFBP-5 expression increased both cell number and DNA synthesis in BxPC-3 cells, but reduced cell number in PANC-1 cells. Consistent with this observation, cell cycle analysis of IGFBP-5-expressing cells revealed accelerated cell cycle progression in BxPC-3 and G2/M arrest of PANC-1 cells. Signal transduction analysis revealed that Akt activation was increased in BxPC-3, but reduced in PANC-1 cells that express IGFBP-5. Inhibition of PI3K with LY294002 suppressed extracellular signal-regulated kinase-1 and -2 (ERK1/2) activation in BxPC-3, but enhanced ERK1/2 activation in PANC-1 cells that express IGFBP-5. When MEK1/2 was blocked, Akt activation remained elevated in IGFBP-5 expressing PaC cells; however, inhibition of PI3K or MEK1/2 abrogated IGFBP-5-mediated cell survival.CONCLUSION: These results indicate that IGFBP-5 expression affects the cell cycle and survival signal pathways and thus it may be an important mediator of PaC cell growth.展开更多
文摘目的探讨细胞S相激酶相关蛋白(S-phasekinase associated protein 2,Skp2)、p27蛋白与喉鳞状细胞癌(简称喉癌)各临床因素及预后的相关性。方法采用免疫组化SP法检测79例喉癌患者肿瘤组织的Skp2、p27表达。结果喉癌中Skp2高表达率(53.16%)显著高于正常喉组织(0%,P<0.05);喉癌Skp2蛋白低表达组的5年生存率(72.18%)显著高于高表达组(44.17%,P<0.01)。p27蛋白在喉癌和癌旁喉组织中的高表达率分别为30.38%和90%,差异具有显著性(P<0.05);喉癌p27蛋白高表达组的5年生存率(72.98%)显著高于低表达组(51.13%,P<0.01)。将Skp2和p27结合分析,Skp2高表达并p27低表达组的5年生存率最低,与另一组相比具有显著性差异(P=0.001)。结论Skp2蛋白通过降解靶蛋白p27可能在喉癌发生、发展中发挥重要作用。
文摘目的分析第10号染色体缺失的磷酸酶及张力蛋白(phosphatase and tensin homolog deleted on chro-mosome ten,PTEN)、基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)、细胞周期蛋白依赖性激酶抑制蛋白27(cyclin dependent kinase inhibitor protein 27,p27^(kip1))在乳腺癌组织中的表达情况,讨论其在乳腺癌发生、发展中的意义。方法选取2014年2月至2016年2月本院肿瘤科和乳腺外科收治的55例乳腺癌患者(乳腺癌组)和35例乳腺良性病变患者(乳腺良性病变组)为研究对象。采用免疫组织化学SP法检测入选患者PTEN、MMP-9、p27^(kip1)的表达水平。结果乳腺良性病变组PTEN和p27^(kip1)的表达率(82.86%,85.71%)均显著高于乳腺癌组(45.45%,43.64%)(P<0.05),MMP-9的表达率(42.86%)显著低于乳腺癌组(69.09%)(P<0.05)。乳腺癌组织中PTEN的表达与MMP-9的表达呈负相关(r=-0.587,P<0.05),与p27^(kip1)的表达呈正相关(r=0.532,P<0.05)。结论 PTEN与p27^(kip1)表达异常可能与乳腺癌的发生、发展及预后相关。MMP-9参与乳腺癌的发生、发展,可作为评估乳腺癌浸润和转移的生物学指标。
基金Supported by A grant from the Arkansas Master Tobacco Settlement and Arkansas Biosciences Institute
文摘AIM: To investigate the functional significance of insulin-like growth factor binding protein-5 (IGFBP-5) overexpression in pancreatic cancer (PaC).METHODS: The effects of IGFBP-5 on cell growth were assessed by stable transfection of BxPC-3 and PANC-1 cell lines and measuring cell number and DNA synthesis. Alterations in the cell cycle were assessed by flow cytometry and immunoblot analyses. Changes in cell survival and signal transduction were evaluated after mitogen activated protein kinase and phosphatidylinositol 3-kinase (PI3K) inhibitor treatment.RESULTS: After serum deprivation, IGFBP-5 expression increased both cell number and DNA synthesis in BxPC-3 cells, but reduced cell number in PANC-1 cells. Consistent with this observation, cell cycle analysis of IGFBP-5-expressing cells revealed accelerated cell cycle progression in BxPC-3 and G2/M arrest of PANC-1 cells. Signal transduction analysis revealed that Akt activation was increased in BxPC-3, but reduced in PANC-1 cells that express IGFBP-5. Inhibition of PI3K with LY294002 suppressed extracellular signal-regulated kinase-1 and -2 (ERK1/2) activation in BxPC-3, but enhanced ERK1/2 activation in PANC-1 cells that express IGFBP-5. When MEK1/2 was blocked, Akt activation remained elevated in IGFBP-5 expressing PaC cells; however, inhibition of PI3K or MEK1/2 abrogated IGFBP-5-mediated cell survival.CONCLUSION: These results indicate that IGFBP-5 expression affects the cell cycle and survival signal pathways and thus it may be an important mediator of PaC cell growth.
