MiR-486-3p targeting ECM1 represses cell proliferation and metastasis in cervical cancer

MicroRNAs (miRNAs) regulate gene expression and are involved in cervical cancer. But the molecular mechanism is still unclear. Here, miRNA profile of cervical cancer was performed and demonstrated that miR-486-3p decreased in specimens of cervical cancer patients. In addition, our clinical data show that decreased miR-486-3p was associated with metastasis in cervical cancer patients. ECM1 was predicted and velified as a target gene of miR-486-3p. Overexpression of miR-486-3p inhibited cell growth and metastasis by targeting ECM1. In a conclusion, these findings suggest that miR-486-3p is a tumor suppressor miRNA and induction of miR-486-3p is a potential strategy to inhibit cervical cancer progression.     

miR-429在膀胱癌中的表达及作用机制

目的探讨miR-429在膀胱癌中的表达及作用机制。方法选取广东省内三家医院2014年1月~2016年12月期间收集的膀胱癌标本120例,同时选取距离肿瘤边缘大于2 cm的癌旁组织作为对照。SYBR green实时荧光定量PCR法检测miR-429在膀胱癌、癌旁组织中的相对表达量,并分析miR-429与临床相关参数的关系,同时观察miR-429过表达或者敲除时T24细胞（膀胱癌细胞系）增殖和凋亡情况。结果膀胱癌组织miR-429的相对表达水平高于正常膀胱组织（P<0.05）;miR-429的表达水平与膀胱癌的肿瘤大小、有无淋巴结转移,及TNM分期有关（P<0.05）;肿瘤直径大于5 cm组miR-429的表达水平高于肿瘤直径小于5 cm组;有淋巴结转移的膀胱癌组miR-429的表达水平高于无淋巴结转移的膀胱癌组;Ⅲ+Ⅳ期膀胱癌组miR-429的表达水平高于Ⅰ+Ⅱ期膀胱癌（P<0.05）。miR-429的表达水平与膀胱癌患者的年龄、性别无关（P>0.05）。miR-429过表达时,膀胱癌细胞（T24细胞系）增殖增加,凋亡减少;而miR-429敲除时,膀胱癌细胞（T24细胞系）增殖减少,凋亡增加。结论miR-429在膀胱癌的发生发展中起着重要作用,其表达水平对膀胱癌的严重程度及预后情况具有一定的参考价值。     

c-Myc转录上调长链非编码RNA ZEB1-AS1促进结直肠癌细胞增殖

目的探讨长链非编码RNA ZEB1-AS1在结直肠癌中高表达的机制及其在结直肠癌中的作用。方法实时荧光定量PCR检测结直肠癌细胞和组织中ZEB1-AS1的表达,分析其表达量与患者预后的相关性。生物信息学预测ZEB1-AS1转录因子结合位点,双荧光素酶报告基因进行转录因子验证。MTS方法检测ZEB1-AS1对结直肠癌细胞增殖能力的影响。结果ZEB1-AS1在结直肠癌细胞和组织中高表达,且与结直肠癌患者较差的预后正相关。转录因子c-Myc在ZEB1-AS1启动子上有一个结合位点。过表达c-Myc转录上调ZEB1-AS1的表达,反之亦然。MTS结果显示过表达ZEB1-AS1促进结直肠癌细胞增殖,而敲低ZEB1-AS1则抑制该细胞的增殖能力。结论c-Myc转录上调ZEB1-AS1,进而促进结直肠癌进程。c-Myc/ZEB1-AS1或许可作为结直肠癌治疗的潜在靶标。     

CRKL knockdown promotes in vitro proliferation,migration and invasion,in vivo tumor malignancy and lymph node metastasis of murine hepatocarcinoma Hca-P cells

Our previous study (Biomed Pharmacother 2015;69:11) demonstrated that the over-expression of CRKL, a chicken tumor virus number 10 regulator of kinase-like protein, suppresses in vitro proliferation, invasion and migration of murine hepatocarcinoma Hca-P cell, a murine HCC cell with lymph node metastatic (LNM) rate of ∼25%. In current work, we investigated the effects of CRKL knockdown on the in vitro cell proliferation, migration and invasion, and on the in vivo tumor malignancy and LNM rate and level for Hca-P cells. Western blotting assay indicated that CRKL was down-regulated by ∼90% in a monoclonal CrkL-shRNA-transfected Hca-P cells. Compared with Hca-P and unrelated-shRNA-transfected Hca-P cell, the in vitro proliferation, migration and invasion potentials were significantly enhanced following CRKL stable deregulation. CRKL knock-down significantly promoted the tumorigenicity malignancy, LNM rates and level of Hca-P-transplanted mice. Consistent with our previous work, it can be concluded CRKL plays an important role in hepatocarcinoma cell proliferation, invasion and migration as well hepatocarcinoma malignancy and metastasis. It functions as a potential tumor suppressor in hepatocarcinoma.     

Paeoniflorin inhibits proliferation and invasion of breast cancer cells through suppressing Notch-1 signaling pathway

Paeoniflorin (PF), one of the major active ingredients of Chinese peony, was reported to possess anti-tumor effect. However, the role of PF in breast cancer remains to be clarified. Therefore, in this context, the present study investigated the effects of PF on breast cancer cell proliferation and invasion, as well as the underlying mechanism. Our results found that PF suppressed the proliferation and invasion of breast cancer cells. We further demonstrated that PF down-regulated the expression of Notch-1; in addition, overexpression of Notch-1 reversed PF-inhibited proliferation and invasion, and knockdown of Notch-1 enhanced PF-inhibited proliferation and invasion in breast cancer cells. In conclusion, the present study suggests that PF inhibits proliferation and invasion of breast cancer cells through suppressing Notch-1 signaling pathway. Therefore, PF may represent a chemopreventive and/or therapeutic agent in the prevention of breast cancer.     

miR-34a通过调控YY1抑制肾癌细胞的增殖及侵袭

目的探讨miR-34a在肾癌组织中表达、miR-34a对人肾癌ACHN细胞增殖和侵袭的影响及调控机制。方法实时聚合酶链反应(PCR)检测miR-34a在20例肾癌及癌旁组织中的表达;采用脂质体转染法将miR-34a mimics转染入肾癌ACHN细胞中,试验分空白对照组、阴性对照组、miR-34a mimics转染组。实时PCR检测转染24 h后miR-34a表达量;噻唑蓝(MTT)试验检测细胞增殖;流式细胞术检测细胞周期;Transwell及Matrigel检测细胞侵袭能力;实时PCR和蛋白质印迹(Western blot)技术检测转染后转录因子YY1表达水平。结果与癌旁组织相比,20例癌组织中miR-34a平均表达量为1.06±0.67,显著低于癌旁组织(1.62±0.83,P<0.01);转染后24 h,miR-34a mimics转染组的miR-34a表达量为157.04±13.01,较阴性对照组显著上调(P<0.01);miR-34a mimics转染组细胞增殖能力显著降低(P<0.01),细胞生长被阻滞在G0/G1期;细胞侵袭能力明显减弱(P<0.01);转染miR-34a mimics后YY1基因在mRNA表达无明显变化(P>0.05),蛋白水平下调。结论 miR-34a在肾癌中低表达,可能与肾癌的发生有关;miR-34a调控YY1的表达可能是抑制肾癌细胞生物活性的重要机制之一。     

miR-205对人胃癌细胞株SGC7901增殖的抑制作用

摘要：目的：观察miR-205对人胃癌细胞株SGC7901增殖的影响及可能的机制。 方法：miR-205 mimics转染SGC7901细胞后,观察其增殖能力;SYBR Green I实时荧光定量PCR检测miR205的表达水平;RT-PCR检测细胞ZEB1和ZEB2的基因表达水平。 结果：与空白对照组miR-205表达的相对水平（0.000 619±0.000）及阴性片段对照组（0.001 064±0.001）相比,miR-205 mimics处理组(0.027 33±0.014)miR205表达水平明显增高（q分别为5.77和5.67,P均<0.01）,而SGC7901细胞的克隆形成能力明显下降,ZEB1和ZEB2 mRNA明显下调。 结论：miR-205可抑制胃癌细胞增殖,其机制可能与下调ZEB1和ZEB2基因表达有关,对研究胃癌分子诊断与治疗具有重要意义。     

转移性宫颈癌细胞衍生的外泌体miR-21-5p促进宫颈癌侵袭及转移

目的 探讨转移性宫颈癌组织的旁分泌作用对肿瘤细胞扩散的影响。方法 选择22例转移性宫颈鳞癌患者的手术标本（癌组织和癌旁组织）和血清标本,以及22名健康体检者的血清标本,采用逆转录-实时荧光定量PCR（RT-qPCR）检测miR-21-5p在癌组织和癌旁组织中的表达水平;分别转染miR-21-5p模拟物/抑制剂到宫颈癌SiHa细胞,采用RT-qPCR、细胞集落形成实验、Transwell迁移实验、噻唑蓝（MTT）比色法、蛋白免疫印迹法、双荧光素酶报告分析差异;采用高速离心法提取血清外泌体;采用纳米颗粒跟踪分析（NTA）技术、蛋白免疫印迹法、透射电子显微镜（TEM）对外泌体进行表征鉴定;采用RT-qPCR 检测宫颈鳞癌患者和健康体检者血清外泌体中miR-21-5p的表达差异;采用受试者操作特征（ROC）曲线分析血清外泌体中miR-21-5p对肿瘤转移的诊断效能。结果 miR-21-5p在转移性宫颈鳞癌组织中表达上调;miR-21-5p过表达能促进宫颈鳞癌SiHa细胞集落形成以及细胞增殖与迁移（P均< 0.01）;双荧光素酶报告显示,miR-21-5p可以靶向快速发育生长因子同源蛋白2抗体（SPRY2）,对SPYR2的表达水平进行调控;miR-21-5p模拟物转染的SiHa细胞中,磷酸化丝裂原和应激激活的蛋白激酶、磷酸化核糖体S6蛋白激酶、磷酸化原癌基因C-RAF、磷酸化丝裂原活化蛋白激酶（MAPK）激酶和磷酸化MAPK蛋白的表达均上调（P均< 0.05）。miR-21-5p在宫颈鳞癌患者的血清外泌体中上调（P < 0.05）。血清外泌体评估宫颈癌转移的ROC曲线下面积为0.9375。结论 转移性宫颈鳞癌患者组织中miR-21-5p通过外泌体传递促进肿瘤转移,其机制可能与靶向SPRY2/细胞外调节蛋白激酶/MAPK信号通路有关。     

MicroRNA-744 inhibited cervical cancer growth and progression through apoptosis induction by regulating Bcl-2

Growing evidence suggests that microRNA plays an essential role in the development and metastasis of many tumor progressions, including cervical cancer. Aberrant miR-744 expression has been indicated in many growth of tumor, the mechanism of miR-744 inhibits both the proliferation and metastatic ability for cervical cancer remains unclear. Accumulating evidences reported that Bcl-2 signal pathway plays an important role in the cellular process, such as apoptosis, cell growth and proliferation. The goal of this study was to identify miR-744 that could inhibit the growth, migration, invasion, proliferation and metastasis of gastric cancer through targeting Bcl-2 expression. Real-time PCR (RT-qPCR) was used to quantify miR-744 expression in vitro and vivo experiments. The biological functions of miR-744 were determined via cell proliferation. Our study indicated that miR-744 targeted on Bcl-2, which leads to the inactivation of apoptosis signaling and the cell proliferation of cervical cancer cells, ameliorating cervical cancer growth and progression. In addition, both up-regulation of miR-744 and down-regulation of Bcl-2 could stimulate Caspase-3 expression, promoting apoptosis of cervical cancer cells. Therefore, our research revealed the mechanistic links between miR-744 and Bcl-2 in the pathogenesis of cervical cancer through modulation of Caspase-3, leading to the inhibition of cervical cancer cell growth. And targeting miR-744 could be served as a novel strategy for future cervical cancer therapy clinically.     

miR-1184 regulates the proliferation and apoptosis of colon cancer cells via targeting CSNK2A1

MicroRNA (miRNA) exerts an important part in colon cancer cell proliferation and apoptosis. Meanwhile, the dysregulation of some miRNAs is detected in colon cancer cells. However, it remains unclear about the underlying mechanism of their effects on tumor pathogenesis. The current work aimed to examine the miR-1184 effect on colon cancer cells. The differentially expressed miRNAs (DEMs), including miR-9-3p, miR-1184, miR-492, miR-92a-1-5p and miR-20a-3p, were obtained from the GSE115108 and GSE132619 data sets using the ‘GEO2R’ online tool. Based on the findings, miR-1184 was significantly down-regulated within colon cancer cells and tissues. Moreover, the experimental results of CCK8, flow cytometry, colony formation and Western blotting assays showed that, miR-1184 over-expression suppressed colon cancer cell proliferation through inhibiting Ki67 expression and promoted their apoptosis through up-regulating cleaved caspase-3 and down-regulating Bcl-2 expression. By contrast, miR-1184 inhibition exerted the opposite effects. A total of 110 target genes of miR-1184 were predicted using the TargetScan and miRTarBase databases, which were then used to construct the protein-protein interaction (PPI) network based on the DAVID and STRING websites and to perform GO and KEGG pathway enrichment analyses. The MCODE plug-in of cytoscape was utilized to verify that CSNK2A1 was the target gene and key gene in significant modules. MiR-1184 directly targets CSNK2A1 via using RNA immunoprecipitation assay and luciferase reporter gene assay. According to the results, CSNK2A1 over-expression reversed the functions of miR‐1184 over-expression in suppressing colon cancer cell proliferation and enhancing their apoptosis. In conclusion, over-expression of miR-1184 inhibits colon cancer cell proliferation but promotes their apoptosis through down-regulating CSNK2A1 expression.     

The inhibitory effects of carnosic acid on cervical cancer cells growth by promoting apoptosis via ROS-regulated signaling pathway

Cervical cancer has been the fourth most common cancer killing many women across the world. Carnosic acid (CA), as a phenolic diterpene, has been suggested to against cancer, exerting protective effects associated with inflammatory cytokines. It is aimed to demonstrate the therapeutic role of carnosic acid against cervical cancer and indicate its underlying molecular mechanisms. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) was performed to assess the possible anti-proliferative effects of carnosic acid. And also, colony formation was used to further estimate carnosic acid’s ability in suppressing cervical cancer cells proliferation. Flow cytometry assays were performed here to indicate the alterations of cervical cancer cells cycle and the development of apoptosis. Western blot assays and RT-PCR were also applied to clarify the apoptosis-associated signaling pathways affected by reactive oxygen species (ROS) generation. And immunofluorescence was used to detect ROS-positive cells. In vivo experiments, CaSki xenograft model samples of nude mice were involved to further elucidate the effects of carnosic acid. In our results, we found that carnosic acid exerted anti-tumor ability in vitro supported by up-regulation of apoptosis and ROS production in cervical cancer cells. Also, acceleration of ROS led to the phospharylation of (c-Jun N-terminal kinase (JNK) and its-related signals, as well as activation of Endoplasmic Reticulum (ER) stress, promoting the progression of apoptosis via stimulating Caspase3 expression. The development and growth of xenograft tumors in nude mice were found to be inhibited by the administration of carnosic acid for five weeks. And the suppressed role of carnosic acid in proliferation of cervical cancer cells and apoptosis of nude mice with tumor tissues were observed in our study. Taken together, our data indicated that carnosic acid resulted in apoptosis both in vitro and vivo experiments via promoting ROS and activating JNK signaling pathways in human cervical cancer cells, which supplied a potential therapy for the application of carnosic acid in clinical treatment.     

The effects of HAART on the expression of MUC1 and P65 in a cervical cancer cell line,HCS-2

Cervical cancer is the third most commonly diagnosed cancer globally and it is one of three AIDS defining malignancies. Highly active antiretroviral therapy (HAART) is a combination of three or more antiretroviral drugs and has been shown to play a significant role in reducing the incidence of some AIDS defining malignancies, although its effect on cervical cancer is still unclear. The aim of this study was to investigate the relationship between cervical cancer and HAART. This was achieved by studying the expression of two signalling molecules expressed in cervical cancer; MUC1 and P65. Following the 24-hour treatment of a cervical cancer cell line, HCS-2, with drugs, which are commonly used as part of HAART at their clinical plasma concentrations, real-time qPCR and immunofluorescence were used in order to study gene and protein expression. A one-way ANOVA followed by a Tukey-Kramer post-hoc test was conducted using JMP 11 software on both sets of data. The drug classified as a protease inhibitor (PI) (i.e. LPV/r) reduced MUC1 and P65 gene and protein expression more than the other drug tested. PIs are known to play a significant role in cell death; therefore, the cells were thought to be more susceptible to cell death following treatment with PIs. In conclusion, the drugs used, especially the PI showed some anticancer effects by facilitating cell death through decreased gene and protein expression of MUC1 and P65 and present promising agents for cancer treatment.     

Survivin和MMP-2在老年宫颈癌的表达及与肿瘤侵袭转移的关系

目的探讨Survivin和基质金属蛋白酶-2(MMP-2)在老年宫颈癌的表达及与肿瘤侵袭转移的关系。方法选择72例老年宫颈上皮内瘤病变(CIN)患者及58例老年宫颈癌患者为研究对象,采用免疫组织化学方法检测患者病变组织Survivin和MMP-2的表达。比较CIN患者与宫颈癌患者Survivin和MMP-2表达阳性率的差别,并探讨Survivin和MMP-2与老年宫颈癌肿瘤侵袭转移的关系。结果 CINⅠ～Ⅱ级、CINⅢ级及宫颈癌患者Survivin和MMP-2阳性率依次升高(P<0.05);Survivin和MMP-2阳性率与FIGO分期、淋巴转移、间质浸润有关(P<0.05)。结论不同级别宫颈病变Survivin和MMP-2阳性率不同,Survivin和MMP-2在老年宫颈癌患者肿瘤侵袭转移等生物学行为中起重要作用。     

高强度超声对荷U14宫颈癌小鼠脾细胞Th1/Th2亚群的影响

目的探讨高强度超声（HIU）对荷U14宫颈癌小鼠脾细胞Th1／Th2亚群的影响。方法将32只雌性BALB／c小鼠随机分为HIU治疗组、手术治疗组、荷瘤对照组及正常对照组，每组8只。各组于种植肿瘤或生理盐水后第7天，分别接受相应治疗；于第17天制备并培养小鼠脾淋巴细胞，收集上清液，应用双抗夹心酶联免疫吸附试验（ELISA）检测各组小鼠脾淋巴细胞分泌的细胞因子IL-2、IFN-γ和IL-4的浓度。结果受刀豆球蛋白A（Con A）刺激时，HIU治疗组IL-2浓度为（1110．13±338．10）pg／ml，较手术治疗组[（641．50±93．29）pg／ml]、荷瘤对照组[（215．75±62．54）pg／ml]明显增高（P〈0．05）；HIU治疗组IFN-γ浓度为（64984．86±9778．80）pg／ml，较荷瘤对照组[（42613．75±4050．75）pg／ml]明显增高（P〈0．05）；HIU治疗组IL-4浓度为（224．94±55．89）pg／ml，较手术治疗组[（330．56±94．63）pg／ml]、荷瘤对照组[（418．13±104．78）pg／ml]明显减少（P〈0．05）。未受ConA刺激时，HIU治疗组IL-2浓度为（1099．25±233．51）pg／ml，较手术治疗组[（241．00±35、44）pg／ml]、荷瘤对照组[（136．75±37．52）pg／ml]、正常对照组[（277．50±57．59）pg／ml]明显增高（P〈0．05）；HIU治疗组IFN-γ浓度为（45390．00±9961．26）pg／ml，较荷瘤对照组[（33662．50±14111．99）pg／ml]明显增高（P〈0．05）。结论HIU固化的U14肿瘤细胞可能激活机体免疫功能，促使其由Th2占优势向Th1占优势逆转，从而提高小鼠抗肿瘤免疫功能，抑制肿瘤生长。     

PRPS2在宫颈癌组织中的表达水平及抑癌机制分析

目的 分析磷酸核糖焦磷酸合成酶2(PRPS2)在宫颈癌中的表达情况及抑癌作用。方法 上海市崇明区第三人民医院采集的66例宫颈癌患者癌组织及20份癌旁组织(距癌组织> 1 cm)标本,免疫组化法检测宫颈癌组织及癌旁组织PRPS2表达;并选择宫颈癌He La细胞,脂质体转染PRPS2小干扰序列(He La-PRPS2组),并设计He La-NC对照组(转染无关siRNA序列)。蛋白印迹法(WB)测定PRPS2干扰效率,四甲基偶氮唑盐法(MTT)检测细胞增殖情况,Transwell侵袭实验检测细胞侵袭能力,流式细胞仪测定细胞凋亡情况,总结PRPS2抑癌机制。结果 ①宫颈癌癌组织PRPS2阳性率为75. 76%,高于癌旁组织25. 00%(P <0. 05);②He La-PRPS2组PRPS2蛋白表达量低于He La-NC对照组(P <0. 05);③He La-NC对照组干扰不同时间增殖活性均高于He La-PRPS2组(P <0. 05);④He La-NC对照组穿膜细胞比率高于He La-PRPS2组(P <0. 05);⑤转染后He La-NC对照组G0/G1期细胞比率高于He La-PRPS2组(P <0. 05),G2/M期细胞比率低于He La-PRPS2组(P <0. 05),细胞凋亡率低于He La-PRPS2组(P <0. 05)。结论宫颈癌癌组织PRPS2呈过表达,沉默宫颈癌细胞株He La PRPS2表达后细胞增殖、侵袭能力降低,细胞凋亡率增加,推测沉默PRPS2表达存在抑癌效应。     

萘普生对体外宫颈癌细胞增殖和凋亡的影响

目的:探讨萘普生对人子宫颈癌Hela细胞增殖和凋亡的影响。方法:用含不同浓度的萘普生细胞培养液(1、10、100、300、500μg/mL)于不同作用时间(6、12、24、48h)处理宫颈癌Hela细胞48h后,采用MTT法检测不同浓度的萘普生细胞培养液在不同作用时间下对Hela细胞增殖率的影响;用500μg/mL的萘普生细胞培养液处理宫颈癌Hela细胞48h后荧光显微镜观察细胞形态变化,并采用Annexin V-FITC/PI染色,以流式细胞仪测定细胞凋亡率。结果:(1)MTT法显示,不同浓度的萘普生细胞培养液对Hela细胞均有抑制作用,不同药物浓度组在同一作用时间下对Hela细胞生长抑制率的差异有统计学意义(P<0.01),同一药物浓度在不同作用时间组之间的细胞生长抑制率的差异也有统计学意义(P<0.01)。(2)Hoechst33342染色后,经荧光显微镜观察,可见到染色质浓缩及凋亡小体等凋亡特征。(3)流式细胞仪检测显示萘普生处理宫颈癌Hela细胞48h后,细胞凋亡率明显增加。结论:萘普生在体外对Hela细胞增殖具有抑制作用,且抑制作用呈时间依赖性及浓度依赖性。     

EBV、ERK1、Ki67在不同临床分型宫颈癌中的表达及其相关性

目的研究EBV、ERKl和Ki67在同临床分型宫颈癌中的表达及相互关系,以探讨宫颈癌的发病机制及其临床意义。方法选择经手术治疗、有明确病理诊断的宫颈癌患者共109例,其中Ⅰ期31例,Ⅱ期14例,Ⅲ期37例和Ⅳ期27例,使用免疫组织化学染色法检测EBV的表达、ERKl和Ki67的表达。同时选取30例正常宫颈石蜡切片作为对照组。结果 EBV、ERKl和Ki67表达随着宫颈癌临床分型而逐渐增加,与0期和Ⅰ期相比,差异均有统计学意义,P<0.05。结论 EBV感染可能是宫颈癌发生原因之一,ERKl的表达以及Ki67可作为评价宫颈癌的发生、发展中的重要指标。     

宫颈癌中多药耐药1基因的表达和意义

目的探讨多药耐药1基因在宫颈癌中表达及其临床意义。方法应用荧光定量PCR法检测42例宫颈癌组织及10例正常宫颈组织中多药耐药1基因mRNA的表达情况。结果宫颈癌组织中多药耐药基因1 mRNA表达(0.573±0.320)明显高于正常宫颈组织(0.186±0.099)(P<0.001);宫颈癌组织中多药耐药基因1 mRNA表达高中分化组(0.678±0.269)高于低分化组(0.383±0.325)(P<0.05),在其他临床病理相关因素上差异无统计学意义(P>0.05)。结论多药耐药1基因在宫颈癌的原发性多药耐药中可能起重要作用,检测多药耐药1基因的表达情况对预测宫颈癌的化疗效果、协助临床选择化疗方案有一定意义。     

HPV L1衣壳蛋白在不同宫颈病变的表达及临床意义

目的 探讨人乳头状瘤病毒（human papillomavirus,HPV）L1衣壳蛋白在不同宫颈病变脱落细胞中的表达及临床意义.方法 收集2012年1月至2013年7月在我院经第二代杂交捕获法检测HPV DNA阳性患者的宫颈脱落细胞标本312份,采用CytoReact HPV L1试剂盒检测壳蛋白在宫颈脱落细胞中的表达,并追踪其组织病理结果.结果 HPV L1衣壳蛋白定位于细胞核,阳性细胞其细胞核着色为红褐色颗粒,位于鳞状细胞的表层,基底细胞无表达.312份宫颈液基细胞学标本中有105份HPV L1衣壳蛋白呈阳性表达,总阳性率为33.65％（105/312）,其中未见上皮内病变或恶性细胞（negative for intraepithelial lesion or malignancy,NILM）为27.33％ （47/172）;未明确意义的非典型鳞状上皮细胞（atypical squamous cell of undermined significance,ASC-US）为36.92％（24/65）;不排除高度鳞状上皮病变的非典型鳞状上皮细胞（ASC of can not exclude high-grade squamous intraepithelial lesion,ASC-H）为21.43％（3/14）;低度鳞状上皮内病变（low-grade squamous intraepithelial lesion,LSIL）为69.44％（25/36）;高度鳞状上皮内病变（high-grade squamous intraepithelial lesion,HSIL）为28.57％（6/21）;鳞癌（squamous cell carcinoma,SCC）为0.00％ （0/4）.六组间HPV L1衣壳蛋白阳性表达率差异有统计学意义（P＜0.05）,其中LSIL与HSIL相比,ASC-US/LSIL与ASC-H/HSIL相比,LSIL与HSIL/SCC相比,LSIL/ASC-H与HSIL/SCC相比,NILM与LSIL相比,HPV L1衣壳蛋白阳性表达率差异均有统计学意义（P均＜ 0.05）,且随宫颈细胞学病变程度的加重,HPV L1衣壳蛋白表达呈下降趋势.312例患者中有143例追踪到组织学结果,其中HPV L1衣壳蛋白阳性表达的有46例,总阳性率为32.17％ （46/143）,其中慢性宫颈炎为27.08％（13/48）,宫颈上皮内瘤样病变Ⅰ级（cervical intraepithelial neoplasia Ⅰ,CIN Ⅰ）为48.84％（21/43）,CINⅡ为33.33％ （8/24）,CINⅢ为17.39％ （4/23）,SCC为0.00％（0/5）.五组间HPVL1衣壳蛋白阳性表达率差异有统计学意义（P＜0.05）.CIN Ⅰ与CINⅡ/CINⅢ相比,慢性宫颈炎与CIN Ⅰ相比HPV L1衣壳蛋白阳性率差异均有统计学意义（P均＜0.05）,且随宫颈组织学病变程度加重,HPVL1衣壳蛋白表达呈下降趋势.以30岁为界将患者分为两组,其中≤30岁组HPV L1衣壳蛋白阳性率为44.00％（44/100）;＞30岁组HPV L1衣壳蛋白阳性率为28.77％（61/212）,两组间差异有统计学意义（P＜0.05）.结论 随宫颈病变程度加重,HPV L1衣壳蛋白表达呈下降趋势,HPV L1衣壳蛋白检测对宫颈鳞状上皮内病变有一定的预测作用.