Expression and Clinical Significance of p27kip1 Protein in Primary Liver Cancer

Summary: To investigate the expression and clinical significance of p27kip1 protein in primary liver cancer, the expression of p27kip1 protein and the relationship with clinicopathological factors were studied in primary liver cancer by using SABC immunohistochemical staining in specimens of 40 cases of primary liver cancer and 20 cases of liver cirrihosis. Our results showed that positive expression rate of p27kip1 protein in primary liver cancer was 37.5 % (15/40), which was lower than that in benign lesion of liver 80.0 % (16/20, P<0.01). The expression level of p27kip1 protein in primary liver cancer showed significant differences in tumor size, Edmonson histological grade, portal invasion, lymph node metastasis, TNM stage (P<0.05, for all), but not significantly correlated with patient's age and histological types. Log rank test showed that the p27kip1 expression was significantly related with prognosis of the patients (P<0.05), and the prognosis of the patients with p27kip1 positive expression was markedly better than that of those with p27kip1 negative expression. It is concluded that the expression of p27kip1 was significantly related clinicopathological factors of primary liver cancer. p27kip1 protein may be used as a novel tumor marker for primary liver cancer.

Expression of p27Kip1, A Cell Cycle Repressor Protein with Dual Roles for Both Cancer Prevention and Promotion, Is Regulated Primarily at the Level of Unusual p27Kip1 mRNA—A Short Concept Proposal

The p27Kip1 is a cell cycle repressor protein that regulates primarily the cell cycle transition from G1 to S phase and hence the DNA replication is in the S phase and cell division in the M phase. Expression of p27Kip1 protein has dual roles for both cancer prevention and promotion. For example, numerous nutritional and chemopreventive anti-cancer agents specifically increase the expression of p27Kip1 protein without directly affecting the expression of any other cell cycle regulatory proteins. On the other hand, pro-cancer agents (like glucose, insulin and other growth factors frequently seen in obesity and/or diabetes) specifically decrease the expression of p27Kip1 protein without directly affecting the expression of any other cell cycle regulatory proteins. Unlike expression of any other cell cycle regulatory proteins, expression of p27Kip1 protein is very unusual. The mRNA of p27Kip1 has a very long and unusual 5’-untranslated region (from -575 to -1 in human). It appears that the 5’-untranslated region of p27Kip1 mRNA forms two alternative secondary structures. One increases the expression of p27Kip1 protein when anti-cancer agents are added and another decrease the expression of p27K1p1 when pro-cancer agents are added. For this short concept proposal, Dr. Albert Einstein’s “visualized thought experiments (German: Gedanken experiment)” were used as a fundamental tool for understanding how either anti- or pro-cancer agents bring the primary structure of the 5’-untranslated region of p27Kip1 mRNA into two alternative secondary structures, thereby either increasing or decreasing, respectively, the translation initiation of p27Kip1 protein.

Lower Concentrations of Glucose or Insulin Decrease the Risk of Various Types of Cancer in the Long-Lived Ames Dwarf Mouse by Increasing the Expression of p27Kip1, a Cell-Cycle Repressor Protein

Introduction. The molecular biological mechanism of the increased incidence of the various types of cancer in obesity or type 2 diabetes in rodents or humans has largely been resolved in recent years. By contrast, the molecular biological mechanism of the decreased, not increased, incidence of the various types of cancer in the homozygous long-lived Ames dwarf mice still remains unresolved. Objective. The first objective of the present study was to investigate whether the decrease in the incidence of cancer in the homozygous long-lived Ames dwarf mice is due to the increase, not decrease, in the expression of p27Kip1, a cell cycle repressor protein. The second objective was to investigate whether the decrease in the incidence of cancer in the homozygous long-lived Ames dwarf mice is due to the decrease, not increase, in the levels of glucose or insulin. Methods. To achieve these objectives, we first performed western immunoblot analysis of the hepatic expression of p27Kip1 protein. We then performed, using a human breast cancer cell line in vitro, the luciferase reporter plasmid assay to determine whether the translation initiation activity of the p27Kip1 mRNA is increased when the concentrations of either glucose or insulin are decreased. Results and Conclusion. The results of the first objective indicated that the hepatic expression of p27Kip1 protein was up-regulated in the homozygous long-lived Ames dwarf mice as expected. We also found that the lower concentrations of glucose or insulin increased the translation initiation activity of the p27Kip1 mRNA.

p27kip1蛋白在卵巢上皮癌中的表达及其临床意义

目的 :研究p2 7kip1在卵巢上皮癌中的表达及其临床意义。方法 :采用免疫组化SP法检测 2 0例卵巢良性、5 8例卵巢恶性上皮性肿瘤中p2 7kip1蛋白的表达。应用Kaplan Meier法及Cox比例风险回归模型 ,分析p2 7kip1蛋白表达与卵巢上皮癌患者预后的关系。结果 :(1)卵巢良性和恶性上皮性肿瘤中p2 7kip1蛋白表达阳性率分别为75 .0 % ,4 6 .6 % ,恶性肿瘤中p2 7kip1蛋白表达阳性率明显低于良性肿瘤 ,恶性肿瘤染色阳性部位以胞浆为主 ;(2 )p2 7kip1蛋白的表达与病理学分级有关 ,与年龄、临床分期、淋巴结转移、组织学亚型无关 ;(3)卵巢上皮癌中 ,p2 7kip1蛋白的表达与bax蛋白的表达呈正相关 ,与bcl 2蛋白的表达呈负相关 ,与ki6 7蛋白无明显相关性 ;(4)p2 7kip1蛋白表达是影响卵巢上皮癌患者预后的独立因素 ,阳性者预后较好。结论 :p2 7kip1蛋白可能与卵巢上皮癌的发生有关。p2 7kip1蛋白可作为判断患者预后的指标。

p27kip1在星形细胞瘤中表达的意义

目的 检测p2 7kip1在星形细胞瘤中的表达并探讨其在星形细胞瘤发生、发展中的作用。方法 采用免疫组化S P法检测了 5 9例星形细胞瘤的表达。结果 p2 7kip1在星形细胞瘤良性组 (Ⅰ级、Ⅱ级 )表达阳性率 76 9% (30 / 39)高于恶性组(Ⅲ级、Ⅳ级 ) 5 0 0 % (10 / 2 0 ) (P <0 0 5 )。p2 7kip1表达水平与星形细胞瘤分级呈负相关 (r =- 0 487,P <0 0 0 0 1)。 结论 细胞周期蛋白依赖性激酶抑制剂p2 7kip1在星形细胞瘤发生、发展中起重要作用 ;p2 7kip1可作为良恶性星形细胞瘤辅助鉴别诊断标记物。

曲古菌素A抑制血清诱导血管平滑肌细胞p27kip1表达的降解

目的:探讨组蛋白去乙酰化酶抑制剂曲古菌素A(TSA)对血管平滑肌细胞(VSMCs)p27kip1表达的影响和调控机制。方法:半定量逆转录聚合酶链反应(RT-PCR)检测p27kip1 mRNA水平,蛋白印迹测定p27kip1和skp2蛋白表达,荧光分光光度法测定20S蛋白酶体活性。结果:100μg/LTSA不影响VSMCs中p27kip1的mRNA水平。100μg/LTSA显著抑制血清诱导的p27kip1蛋白下调,并延长p27kip1蛋白的半衰期。100μg/LTSA抑制血清诱导的skp2表达上调,且skp2表达与相应时点p27kip1蛋白呈负相关。100μg/LTSA对20S蛋白酶体活性物无影响。结论:TSA对VSMCs的p27kip1表达调控不是在转录水平上,而是通过翻译后机制抑制血清诱导VSMCs的p27kip1蛋白降解,其机制可能与TSA抑制泛素连接酶亚单位skp2表达有关。

p27kip1蛋白在宫颈癌及癌前病变中的表达及临床意义

目的:探讨宫颈癌及癌前病变组织中p27kip1蛋白的表达情况及临床意义。方法:采用免疫组化S-P法检测32例宫颈正常鳞状上皮、70例宫颈上皮内瘤样病变(CINⅠ22,CINⅡ24,CINⅢ24)、47例宫颈浸润癌中p27kip1蛋白的表达,分析宫颈癌形成过程中p27kip1蛋白表达的变化以及p27kip1蛋白表达与宫颈癌临床病理特征的关系。结果:p27kip1蛋白在CINIII及宫颈浸润鳞癌中表达平均阳性细胞百分率分别为37.1%,14.3%,显著低于宫颈正常鳞状上皮和CINⅠ、Ⅱ(分别为58.0%,65.9%,62.1%),有统计学意义(P<0.0001)。p27kip1蛋白在不同组织类型、分化程度、临床期别、有无淋巴转移的宫颈浸润癌中的表达无统计学差异。结论:p27kip1蛋白表达下降可能在宫颈细胞的恶性转化过程中起重要作用,为宫颈癌变的早期信号。

曲古菌素A对血管平滑肌细胞p27kip1表达的调控机制研究

目的探讨组蛋白去乙酰化酶抑制剂曲古菌素A(Trichostatin A,TSA)对血管平滑肌细胞(VSMC)的p27kip1表达的影响和调控机制。方法半定量逆转录聚合酶链反应(RT-PCR)检测p27kip1的mRNA水平,蛋白印迹测定p27kip1和S-phase kinase-associated protein-2(skp2)蛋白表达,荧光分光光度法测定20S蛋白酶体活性。结果100 ng/ml TSA不影响VSMC中p27kip1的mRNA水平。100 ng/mlTSA显著抑制血清诱导的p27kip1蛋白下调,并延长p27kip1蛋白的半衰期。100 ng/ mlTSA抑制血清诱导的skp2表达上调,且skp2表达与相应时点p27kip1蛋白呈负相关。100 ng/ml TSA对20S蛋白酶体活性物影响。结论TSA对VSMC的p27kip1表达调控不是在转录水平上,而是通过翻译后机制抑制血清诱导VSMC的p27kip1蛋白降解,其机制可能与TSA抑制泛素连接酶亚单位skp2表达有关。

p27kip1在胃癌中的表达和意义

目的 探讨 p2 7kip1 (细胞周期素依赖性激酶抑制因子 )在胃癌中表达及其与胃癌临床病理学特征的关系。方法 采用免疫组织化学方法检测 p2 7kip1在 60例胃癌组织原发灶和淋巴结转移灶中的表达。结果 p2 7kip1在胃癌的阳性表达率为 43 33% ( 2 6/60 ) ,阳性细胞定位于细胞浆 ,在高分化及Ⅰ ,Ⅱ期胃癌高表达 (P <0 0 5 ) ,且与淋巴结转移密切相关 (P <0 0 1 )。结论 p2 7kip1表达与胃癌组织分化程度、淋巴结转换呈负相关 ;p2 7kip1表达对估计胃癌预后有一定意义。

P13K/Akt/p27kip1通道介导胃癌细胞对阿霉素、足叶乙甙化疗的耐药性及其机制

目的:探讨P13K/Akt(PKB)/p27kipl通道对胃癌细胞BGC-823化疗的效果和作用机制.方法:将培养的胃癌细胞BGC-823分为对照组,P13K/Akt/p27kipl通道抑制剂Wort组(Wort组),足叶乙甙组(Eto组),阿霉素组(Dox组),Eto+Wort组和Dox+Wort组;MTT法检测细胞生存率,流式细胞仪检测细胞周期和凋亡,Western印迹法检测p27Kipl蛋白表达水平,RT-PCR检测p27基因mRNA表达水平.结果:与对照组相比,Wort组,Eto+Wort组和Dox+Wort组24 h细胞生存率降低(57.8%、46.5%、44.3% vs 46.5%、44.3%,P<0.01),G_0-G_1期的比例增多(85.0±3.54,91.5±3.63,92.4±3.64 vs 71.5±3.25,P<0.01),12 h和24 h蛋白表达升高;Eto组和Dox组细胞生成率较对照组升高,但G_0-G_1期的比例无明显变化;各组p27基因mRNA表达水平一致.结论:P13K/Akt/p27通道激活能介导肿瘤细胞化疗耐药.

KLF5介导p27kip1表达对胶质瘤U87细胞增殖和侵袭的影响

目的观察Kruppel样因子5(KLF5)介导p27kip1对胶质瘤U87细胞增殖和侵袭的影响。方法常规培养胶质瘤细胞U87,将其分为si-NC组和si-KLF5组,si-NC组转染对照siRNA,si-KLF5组转染KLF5 siRNA。采用MTS法检测两组细胞增殖能力,流式细胞术检测细胞周期,Boyden实验检测细胞侵袭能力,Western blotting法检测细胞中细胞周期相关蛋白Cyclin D1、CDK4、CDK6和上皮间质转化蛋白Snail1表达。Western blotting检测显示p27kip1在si-KLF5组的表达水平高于si-NC组,故设置si-KLF5+si-p27kip1组和si-NC组、si-KLF5组,si-KLF5+si-p27kip1组给予p27kip1 siRNA与KLF5 siRNA共同转染U87细胞,si-KLF5组转染KLF5 siRNA,si-NC组转染对照siRNA。比较三组细胞的增殖能力和侵袭能力。结果与si-NC组相比,si-KLF5组U87细胞增殖和侵袭能力均降低(P均<0.05),G1期细胞比例增加(P<0.05),细胞中Cyclin D1、CDK4、CDK6和Snail1蛋白表达降低(P均<0.05)。si-KLF5+si-p27kip1组细胞增殖和侵袭能力均较si-NC组降低(P均<0.05),较si-KLF5组增加(P均<0.05)。结论干扰KLF5表达后U87细胞的增殖和侵袭能力降低,其机制与上调p27kip1表达有关。

乳腺癌P27kip1与bcl-2、p53、PCNA蛋白表达及其相关性和预后关系的研究

目的 :研究乳腺癌组织P2 7kip1的表达 ,探讨其与bcl-2、p5 3、PCNA蛋白表达的相关性及患者的预后意义。 方法 :采用免疫组化Envision(二步法 ) ,检测 74例乳腺癌组织P2 7kip1蛋白表达水平 ,其中 5 0例同时做了bcl-2、p5 3、PCNA蛋白免疫组化标记。结果 :本组 74例中 ,P2 7kip1低表达者 43例 ( 5 8% )中生存期≤ 5年 14例 ,死亡率 3 2 5 6% ( 14 /4 3 ) ;高表达者3 1例 ( 4 2 % )中生存期≤ 5年 2例 ,死亡率 6.45 % ( 2 /3 1)。乳腺癌P2 7kip1蛋白表达水平与肿块大小、组织学分级、淋巴结转移、预后等相关 ( P <0 0 5 )。P2 7kip1低表达与bcl-2低表达、P2 7kip1低表达与P5 3高表达以及P2 7kip1低表达与PCNA高表达3组患者的死亡率均高于P2 7kip1蛋白的单一表达者。 结论 :P2 7kip1低度表达者预后较高度表达者差 ,其表达水平可以作为评估预后的有效参考因素 ,而P2 7kip1与其它多种肿瘤预后有关的标记物联合检测更有助于判断乳腺癌的预后。

CacyBP/SIP nuclear translocation regulates p27Kip1 stability in gastric cancer cells

AIM: To investigate the mechanism of calcyclin binding protein/Siah-1 interacting protein(Cacy BP/SIP) nuclear translocation in promoting the proliferation of gastric cancer(GC) cells. METHODS: The effect of Cacy BP/SIP nuclear translocation on cell cycle was investigated by cell cycle analysis. Western blot analysis was used to assess the change in expression of cell cycle regulatory proteins and proteasome-mediated degradation of p27Kip1. Coimmunoprecipitation(co-IP) analysis was performed to examine the binding of Cacy BP/SIP with Skp1. A Cacy BP/SIP truncation mutant which lacked the Skp1 binding site was constructed and fused to a fluorescent protein. Subsequently, the effect on Skp1 binding with the fusion protein was examined by co-IP, while localization of fluorescent fusion protein observed by confocal laser microscopy, and change in p27Kip1protein expression assessed by Western blot analysis.RESULTS: Cacy BP/SIP nuclear translocation induced by gastrin promoted progression of GC cells from G1 phase. However, while Cacy BP/SIP nuclear translocation was inhibited using si RNA to suppress Cacy BP/SIP expression, cell cycle was clearly inhibited. Cacy BP/SIP nuclear translocation significantly decreased the level of cell cycle inhibitor p27Kip1, increased Cyclin E protein expression whereas the levels of Skp1, Skp2, and CDK2 were not affected. Upon inhibition of Cacy BP/SIP nuclear translocation, there were no changes in protein levels of p27Kip1 and Cyclin E, while p27Kip1 decrease could be prevented by the proteasome inhibitor MG132. Moreover, Cacy BP/SIP was found to bind to Skp1 by immunoprecipitation, an event that was abolished by mutant Cacy BP/SIP, which also failed to stimulate p27Kip1 degradation, even though the mutant could still translocate into the nucleus.CONCLUSION: Cacy BP/SIP nuclear translocation contributes to the proliferation of GC cells, and Cacy BP/SIP exerts this effect, at least in part, by stimulating ubiquitin-mediated degradation of p27Kip1.

胶质瘤组织中EGFR、p27^(kip1)的表达变化及意义

目的观察胶质瘤组织中表皮生长因子受体(EGFR)和p27kip1的表达变化,并探讨其临床意义。方法采用免疫组化SP法检测60例胶质瘤组织、5例正常脑组织中EGFR和p27kip1。结果 60例胶质瘤患者中有39例表达EGFR,20例表达p27kip1。EGFR在正常脑组织中无表达,在Ⅱ、Ⅲ、Ⅳ级胶质瘤中阳性表达率分别为52.4%、60.9%、87.5%(P<0.05);p27kip1在正常脑组织中表达率为80.0%,在Ⅱ、Ⅲ、Ⅳ级胶质瘤中阳性表达率分别为57.1%、26.1%、12.5%(P<0.05)。EGFR表达与胶质瘤病理分级呈正相关(r=0.426,P<0.05),p27kip1表达与胶质瘤病理分级呈负相关(r=-0.325,P<0.05)。结论 EGFR、p27kip1表达与胶质瘤的恶性程度有关,其表达异常可能在肿瘤形成中起促进作用。

舌鳞状细胞癌组织中Cks1、Skp2和p27^(kip1)蛋白的表达及其临床意义

目的:检测舌鳞状细胞癌(舌癌)组织中Cks1、Skp2和p27kip1蛋白的表达,分析其与患者临床病理特征的关系,探讨其在舌癌的发生发展及预后中的作用。方法:采用免疫组织化学法检测45例舌癌组织、30例癌旁组织和10例正常舌黏膜组织中Cks1、Skp2和p27kip1蛋白的表达情况;比较不同类型舌组织中各蛋白表达阳性率的差异;分析Cks1、Skp2和p27kip1蛋白表达与舌癌临床病理学参数的关系。结果:在舌癌组织中,Cks1和Skp2蛋白呈强表达,阳性表达率为73.3%和62.2%,在癌旁组织和正常舌黏膜组织中其阳性表达率依次降低,阳性表达率分别为23.3%、10.0%和36.7%、10.0%;在舌癌组织中,p27kip1蛋白表达明显减少或缺失,阳性表达率为24.4%,在癌旁组织中和正常舌黏膜组织中其阳性表达水平依次升高,阳性表达率分别为30.0%和70.0%;在舌癌组织中Cks1和Skp2蛋白阳性表达率高于正常舌黏膜组织和癌旁组织(P<0.05),而p27kip1蛋白阳性表达率低于正常舌黏膜组织和癌旁组织(P<0.05)。舌癌组织中Cks1、Skp2和p27kip1蛋白阳性表达率与舌癌患者的年龄和性别无关联(P>0.05);与癌组织淋巴结转移、TNM分期、分化程度和临床分期有关联(P<0.05)。结论:舌癌组织中Cks1和Skp2蛋白阳性表达率升高、p27kip1蛋白阳性表达率降低,Cks1、Skp2和p27kip1蛋白阳性表达率的检测有助于判断舌癌的恶性程度和预后。

P16^(ink4a)、P27^(kip1)和p21^(waf1)蛋白在肺癌及其淋巴结转移中的表达意义

目的研究三种细胞周期蛋白依赖性激酶抑制因子(CDKI)P16ink4a、P27kip1和p21waf1在75例不同组织学类型肺癌及其配对淋巴结转移癌中的表达意义。方法利用免疫组化方法检测P16ink4a、P27kip1和p21waf1在不同组织学类型、不同分化程度肺癌及其配对淋巴结转移癌中的蛋白表达。结果三种CDKI在75例不同组织学类型肺癌及其配对淋巴结转移癌中均有较高的表达。三种CDKI在高-中分化鳞癌中的表达量均显著高于其在低分化鳞癌中的表达(P<0.05)。P27kip1在高-中分化腺癌中的表达量显著高于其在低分化腺癌中的表达(χ2=7.985,P=0.008)。P27kip1在高分化鳞癌中的细胞浆定位表达明显多于细胞核定位表达(χ2=8.571,P=0.003)。肺癌各种组织学类型均存在两种或两种以上CDKI基因同时表达,鳞癌中P16ink4a的阳性表达与P27kip1的阴性表达存在显著性负相关(P<0.05)。结论三种CDKI的表达与肺鳞癌、腺癌的组织学分化相关,表达量的减少发生于晚期肿瘤发展。肺癌及其淋巴结转移灶中三种CDKI基因共性表达为肺癌的靶向治疗提供前景。

消岩汤对人乳腺癌细胞MCF-7增殖的影响及机制

目的观察消岩汤对人乳腺癌细胞MCF-7增殖的影响,并探讨其机制。方法收集对数生长期MCF-7细胞,分为消岩汤干预组和对照组。对照组加入100μL的DMEM培养基;消岩汤干预组加入100μL消岩汤颗粒剂溶解液,采用梯度药物浓度(0.09、0.045、0.0225μg/μL)的消岩汤分别孵育人乳腺癌细胞MCF-724、36及48 h后,MTT法检测MCF-7细胞增殖抑制率。应用qRT-PCR法、Western blotting法检测消岩汤干预组0.09μg/μL孵育细胞48 h时CCN5表达及下游调控因子Skp2和p27Kip1 mRNA和蛋白表达。结果消岩汤干预组MCF-7细胞增殖受到抑制,并且高浓度(0.09μg/μL)消岩汤孵育48 h细胞增殖抑制率低于24 h(P<0.05);消岩汤干预组(0.09μg/μL,孵育48 h)CCN5 mRNA表达高于对照组,同时,Skp2 mRNA表达低于对照组(P均<0.05),p27Kip1 mRNA高于对照组;消岩汤干预组(0.09μg/μL,孵育48 h)CCN5蛋白表达高于对照组,而Skp2蛋白低于对照组(P均<0.05),p27Kip1蛋白高于对照组(P<0.05)。结论消岩汤可抑制人乳腺癌细胞MCF-7增殖,其机制可能是在mRNA和蛋白水平通过上调CCN5表达、下调Skp2表达和上调p27Kip1表达实现。

Skp2、p27^(Kip1)在胆囊癌组织中的表达及其临床意义

目的探讨Skp2、p27Kip1在胆囊癌及癌旁组织中的表达情况及与其临床病理特征的关系。方法采用免疫组织化学PV6000二步法,检测Skp2、p27Kip1在78例胆囊癌及癌旁组织中的表达情况,并应用SPSS13.0统计软件分析2种生物指标与胆囊癌临床参数的关系。结果 Skp2与p27Kip1在胆囊癌中的阳性表达率分别为59.0%和39.7%,在癌旁组织中为25.0%和70.0%,胆囊癌中Skp2、p27Kip1阳性表达率均高于胆囊癌旁组织(P均<0.05)。Skp2表达与Nevin分期、分化程度及坏死情况相关,Nevin分期高、分化程度低及伴有坏死的患者Skp2表达高(P均<0.05)。p27Kip1阳性表达与患者Nevin分期、神经侵犯及坏死情况呈负相关性,Nevin分期早、无神经侵犯或不伴坏死患者p27Kip1表达水平高(P均<0.05)。相关性检验显示Skp2与p27Kip1两者间无相关性(P>0.05)。结论 Skp2、p27Kip1均与胆囊癌的发生发展有一定关系,可能成为胆囊癌新的临床诊断和监测预后的指标.

乳腺癌细胞三种肿瘤标记物表达及其与临床病理特征相关研究

目的检测肿瘤标记物14-3-3σ、Akt和p27Kip1蛋白在乳腺癌中的表达,分析其与临床病理特征及Her-2的相关性。方法应用免疫组织化学技术（SABC）检测组织中14-3-3σ、Akt和p27Kip1蛋白的表达,结合临床资料和随访资料,进行回顾性研究,作出评估。结果胞浆14-3-3σ、Akt或p27Kip1蛋白胞浆表达均与淋巴结转移和临床分期呈正相关（P〈0.01或P〈0.05）,并提示生存相对较差,Her-2蛋白可能对PI3k-Akt和p27Kip1通路参与乳腺癌致病起到一定作用。结论14-3-3σ、Akt或p27Kip1蛋白可作为判断乳腺癌淋巴转移和预后评估的有效指标。

细胞周期相关蛋白cyclin E、cdk2和p27^(kip1)在垂体腺瘤中的表达

目的观察细胞周期相关蛋白cyclin E、cdk2和p27kip1在垂体腺瘤中的表达情况,探讨其与垂体腺瘤临床生物学行为的关系。方法采用免疫组织化学SP法检测37例非侵袭性垂体腺瘤和21例侵袭性垂体腺瘤组织中cyclin E、cdk2和p27kip1蛋白的表达情况。结果在侵袭性垂体腺瘤中cyclin E和cdk2的表达明显高于非侵袭性垂体腺瘤(均P<0.01),p27kip1的表达明显低于非侵袭性垂体腺瘤(P<0.01);cyclin E与cdk2在垂体腺瘤中的表达呈正相关(r=1,P<0.01),两者与p27kip1的表达呈负相关(均r=-1,P<0.01);cyclin E和cdk2的表达与垂体腺瘤的侵袭性呈正相关(r=0.685,r=0.667,均P<0.01),而p27kip1的表达与垂体腺瘤的侵袭性呈负相关(r=0.659,P<0.01)。结论cyclin E、cdk2及p27kip1的表达情况可以作为判断垂体腺瘤的侵袭性和预后的指标。