ABCG2蛋白在甲状腺乳头状癌中的表达及临床意义

目的 探讨ABCG2蛋白在甲状腺乳头状癌组织中的表达及其临床意义.方法 收集武汉大学人民医院2000-2006年手术切除及活检的甲状腺乳头状癌标本40例和甲状腺腺瘤标本20例.采用免疫组织化学方法检测甲状腺乳头状癌和甲状腺腺瘤组组织内ABCG2蛋白的表达.利用HPIAS-2000图像分析系统测定ABCG2蛋白在甲状腺乳头状癌及甲状腺腺瘤中表达的平均光密度和平均阳性面积率.结果 甲状腺乳头状癌组织中ABCG2蛋白呈高表达;甲状腺腺瘤中ABCG2蛋白呈低表达;图像分析结果显示两组间差异有显著性意义(P＜0.05).结论 ABCG2在甲状腺乳头状癌组织中的高表达可能参与了甲状腺乳头状癌的发生、发展,而且其在癌组织中的高表达可能参与了甲状腺乳头状癌化疗过程中多药耐药形成.     

IGFBP7在甲状腺乳头状癌中的表达及意义

目的观察胰岛素样生长结合蛋白-7(IGFBP7)在甲状腺乳头状癌中的表达及意义。方法对87例甲状腺乳头癌(PTC)组织及癌旁组织(PeT)进行IGFBP7、Ki67、p53免疫组织化学分析,其中10例提取蛋白用半定量western blot方法进行IGFBP7表达水平分析。结果 (1)IGFBP7免疫组化显示,PTC癌组织IGFBP7阳性率达78.16%(68/87),明显高于癌旁组织的31.03%(27/87)(P0.05);(2)Western blot灰度值比较,癌组织IGFBP7表达水平显著高于癌旁组织(t=2.875,P0.05);(3)Ki67、p53与IGFBP7相关性分析显示,p53表达水平与IGFBP7表达水平呈显著正相关性(r=0.261,P0.05),而Ki67表达水平与IGFBP7表达水平无相关性(r=0.148,P=0.170);(4)高水平表达的IGFBP7与PTC淋巴结转移高度相关(r=0.238,P0.05)。结论 IGFBP7表达异常增高可能与甲状腺乳头状癌发生及发展有关,有望成为诊断PTC的一项新型的生物标记物。     

COX-2和IL-1在甲状腺乳头状癌组织中的表达

目的探讨COX-2和IL-1在甲状腺乳头状癌组织中的表达及其在肿瘤的发生和发展中的作用。方法收集武汉大学人民医院和武汉大学中南医院病理科2000-2006年手术切除及活检的甲状腺乳头状癌标本共40例,另取癌周围组织5例作对照。采用免疫组织化学方法观察各组组织内COX-2和IL-1的表达。利用HPIAS-2000图像分析系统测定COX-2和IL-1在癌及癌旁组中表达的平均光密度和平均阳性面积率。结果甲状腺乳头状癌组织中COX-2和IL-1呈高表达;癌旁组织中COX-2和IL-1呈低表达。图像分析结果显示两组间差异有显著性意义（P〈0.01）。结论IL-1可能通过诱导COX-2的表达,在促进肿瘤的发生和发展中起作用。     

HINT2在甲状腺乳头状癌中的表达和功能研究

HINT2与多种肿瘤发生发展密切相关,在甲状腺癌中的功能还不清楚.该文使用组织芯片检测甲状腺乳头状癌组织中HINT2的表达,发现12例癌组织中HINT2蛋白表达水平显著高于正常组织(86％,P＜0.05).该文构建高表达和低表达HINT2的甲状腺乳头状癌细胞系K1稳定克隆后,使用CCK8和克隆形成实验检测HINT2对细...     

Gankyrin在甲状腺乳头状癌的表达及临床意义

采用荧光定量PCR、Western blot及免疫组化方法对比研究gankyrin m RNA及蛋白在甲状腺乳头状癌(papillary thyroid carcinoma,PTC)、桥本氏甲状腺炎(Hashimoto’s thyroiditis,HT)及正常甲状腺组织中的表达情况,分析gankyrin蛋白表达与PTC临床病理特征的关系,探讨gankyrin基因对PTC发生发展的影响。结果显示,PTC及HT样本中gankyrin m RNA及蛋白水平的表达量均高于正常对照组,有统计学显著意义(P0.01);PTC组及HT组间的表达无统计学差异(P0.05);临床特征分析表明,gankyrin蛋白表达在PTC中的表达与患者的性别、年龄、TNM分期等无关,而与是否合并HT有关。Gankyrin基因在PTC及HT中的高表达说明其在这两种关系密切的疾病中扮演着重要的角色,提示其与PTC的分子机制有关。     

DcR3在甲状腺乳头状癌中的表达及临床意义

应用RT-PCR、Westem blot、免疫组化分别检测甲状腺乳头状癌组织与癌旁正常甲状腺组织标本中DcR3mRNA及蛋白的表达情况,探讨DcR3在甲状腺乳头状癌组织中的表达及,临床意义。RT-PCR检测显示,甲状腺乳头状癌中DcR3 mRNA的表达明显高于正常甲状腺组织（P〈0．05）：Western blot提示,DcR3蛋白在甲状腺乳头状癌中表达比正常甲状腺组织高（P〈0．05）;免疫组化显示,DcR3蛋白在甲状腺乳头状癌中高表达（P〈0．05）。DcR3mRNA及蛋白质在甲状腺乳头状癌及正常甲状腺组织间的表达差异有统计学意义（P〈0．05）。DcR3基因及蛋白在甲状腺乳头状癌中高表达,提示DcR3可能促进了甲状腺乳头状癌的发生发展。     

微小RNA-205 在甲状腺乳头状癌中的表达及临床意义

目的:观察微小RNA(microRNA,miRNA,miR)-205在甲状腺乳头状癌(PTC)中的表达并探讨其临床意义。方法:收集自2014年1月至2014年12月在我院甲状腺外科住院治疗的甲状腺乳头状癌患者的术后新鲜病理组织45例,其中男14例,女31例,年龄24-69岁,平均45.5岁。结节性甲状腺肿28例,癌旁正常甲状腺组织5例。提取各组织中的miRNA,应用实时荧光定量聚合酶链反应(RT-q PCR)方法检测miR-205的表达情况。结果:甲状腺乳头状癌miR-205的表达量较非肿瘤组织(结节性甲状腺肿、癌旁组织)明显下调[(1.06±1.76)vs(3.19±4.88),P=0.038]。伴淋巴结转移的PTC组织中miR-205表达量明显低于无淋巴结转移的PTC组织[(1.21±1.80)vs(9.59±1.60),P=0.003]。miR-205的相对表达与PTC患者性别、年龄及浸润与否均无显著相关性,而肿瘤直径呈显著相关性。结论:miR-205在PTC中的表达异常下调,可能与PTC的发生、侵袭和转移有关。     

抑癌基因PTEN 在甲状腺乳头状癌中的表达及临床意义*

目的:通过免疫组织化学方法检测PTEN基因在正常甲状腺组织、甲状腺良性肿瘤组织、甲状腺乳头状癌癌组织中的表达水平并进行比较,探讨其对甲状腺乳头状癌诊断和治疗的意义。方法:采用SP免疫组化方法,用已知阳性组织做阳性对照,以磷酸盐缓冲液(PBS)代替一抗做阴性对照,分别作HE染色和免疫组织化学染色。结果:PTEN蛋白在三组组织中的表达差异具有显著性(P<0.001);正常甲状腺组织、甲状腺良性肿瘤组织中的阳性率分别为100%和82.5%,均显著高于甲状腺癌组织中的45%(P<0.05),即PTEN在甲状腺癌中表达显著降低;PTEN在甲状腺乳头状癌淋巴结转移组和无淋巴结转移组阳性表达率分别为15%和60%,差异有显著性(x2=10.91,P=0.001);PTEN在甲状腺乳头状癌在包膜侵犯组和无侵犯组的阳性表达率分别为25.93%和60.61%,差异有显著性(x2=7.22,P=0.007);PTEN在甲状腺癌淋巴结转移组和包膜侵犯组的阳性表达强度显著低于无淋巴结转移和包膜侵犯组(P<0.01),有统计学意义。结论:PTEN基因表达的降低在甲状腺癌的发生和转移过程中起重要作用。     

NF-κB在甲状腺乳头状癌中的表达及临床意义

探讨NF-κB在甲状腺乳头状癌组织中的表达及其临床意义。采用RT-PCR、蛋白质印迹（Western blot）和免疫组织化学法检测140例甲状腺乳头状癌及其癌旁正常甲状腺组织中NF-κB表达水平,分析其表达水平变化与临床病理特征的关系。结果表明,78.6%（110/140）甲状腺乳头状癌组织NF-κB mRNA表达量明显高于癌旁正常甲状腺组织,80.7%（113/140）甲状腺乳头状癌组织NF-κB蛋白表达量明显高于癌旁正常甲状腺组织,差异具有统计学意义（P<0.01）。免疫组化显示NF-κB的阳性表达主要定位于胞浆,在甲状腺乳头状癌组织的阳性率为81.4%,显著高于癌旁正常甲状腺组织（P<0.01）,NF-κB 表达水平与肿瘤大小、淋巴结转移及临床病理分期有关,但与性别、年龄无关。NF-κB在甲状腺乳头癌组织中高表达,且NF-κB的异常表达与甲状腺乳头状癌的发生、发展及转移密切相关。     

Ezrin蛋白在甲状腺乳头状癌中的表达及其与生存期关系的研究

目的探讨膜细胞骨架链接蛋白Ezrin在甲状腺乳头状癌组织中的表达及其与生存期关系的研究。方法收集武汉大学人民医院和武汉大学中南医院病理2000-2006年手术切除及活检的甲状腺乳头状癌标本40例和甲状腺腺瘤标本20例。采用免疫组织化学方法检测各组组织内Ezrin蛋白的表达。利用HPIAS-2000图像分析系统测定Ezrin蛋白在甲状腺乳头状癌及甲状腺腺瘤中表达的平均光密度和平均阳性面积率,并结合临床资料进行总生存期分析。结果 1.甲状腺乳头状癌组织中Ezrin蛋白呈高表达;甲状腺腺瘤中Ezrin蛋白呈低表达;图像分析结果显示两组间差异有显著性意义(P<0.05)。2.Ezrin蛋白表达强阳性组总生存期均短于表达弱阳性组(P<0.05),差异有统计学意义。结论 Ezrin蛋白与甲状腺乳头状癌的发生、发展及临床预后有密切关系。     

Absent in melanoma 2 suppresses epithelial-mesenchymal transition via Akt and inflammasome pathways in human colorectal cancer cells

Absent in melanoma 2 (AIM2) is a critical component in natural immunity system and is closely related to cancer initiation and development. It has been shown that AIM2 inhibited colorectal cancer (CRC) development and cell proliferation. It remains unresolved how AIM2 acts on CRC metastasis. In this study, we assessed migration, invasion ability, and epithelial-mesenchymal transition (EMT) program upon AIM2 overexpression or knockdown in human CRC cells. Transwell assay demonstrated that upregulation of AIM2 reduced cell migration and invasion. Epithelial marker E-cadherin was augmented and mesenchymal markers vimentin, as well as Snail, were examined decreased by Western blot, real-time polymerase chain reaction, and immunofluorescence. Correspondingly, knockdown of AIM2 led to a reverse consequence. In addition, AIM2 regulated Akt phosphorylation and effects of AIM2 on cell invasion and EMT were recovered after administration of Akt inhibitor, suggesting that AIM2 suppressed EMT dependent on Akt pathway. In addition, caspase-1 inhibitor exposure indicated that AIM2 abrogated EMT through the inflammasome pathway as well. In summary, AIM2 suppressed EMT via Akt and inflammasome pathways in human CRC cells.     

Differential activation of CREB by Akt1 and Akt2

Members of Akt family are highly conserved protein kinase and yet, they show clearly distinct in vivo functions. Here, we have examined the abilities of Akt1 and Akt2 to activate CREB. We found that, in contrast to Akt1 that induces CREB phosphorylation at Ser-133 and CREB target gene expression, Akt2 was unable to induce CREB phosphorylation at Ser-133 in vivo and CREB target gene expression. This difference is specific to CREB as both Akt1 and Akt2 similarly inhibits FoxO1 mediated gene expression. We further showed that the regulatory domain of Akt plays a critical role to confer Akt substrate specificity as substitution of regulatory domain of Akt1 with that of Akt2 abolished the ability of Akt1 to activate CREB. We suggest that the regulatory domain of Akts contributes to the functional difference between Akt1 and Akt2.     

Twist2的生物学功能及其分子机制

碱性螺旋-环-螺旋(Basic helix-loop-helix protein,bHLH)家族成员Twist2对间质细胞系的发生和发育起转录调节作用,经直接或间接机制发挥分子开关功能,从而激活或抑制靶基因。Twist2能直接结合DNA上 E-box保守序列,招募共激活物或抑制剂;能与E蛋白调节因子发生蛋白-蛋白相互作用,干扰激活或抑制功能。Twist2无义突变导致Setleis综合征。对Twist2的早期研究多集中在骨骼发育,随后在多种肿瘤中发现其有表达差异,研究表明Twist2在肿瘤的上皮-间质转化(Epithelial-mesenchymal transition,EMT)中发挥着重要作用。Twist2参与了多条通路的调控,其调控作用的发挥受到时空表达、磷酸化、二聚化和细胞定位的调节,在机体的正常发育、体内平衡和疾病发生机制中研究Twist2的作用显得尤为重要。文章对Twist2在成骨分化、肿瘤形成和EMT中的作用及其分子机制进行综述,以便帮助了解Twist2的生物学功能,为进一步在疾病的诊断、发展、以及治疗等方面的转化应用研究提供依据。     

Expression of obestatin and ghrelin in papillary thyroid carcinoma

Ghrelin and obestatin are two peptide hormones with opposing roles in the control of appetite: orexigenic and anorexigenic, respectively. Loss of appetite is a common, serious complication of many forms of malignancy. The goals of this study were to investigate: (i) whether there are differences in ghrelin and obestatin peptide expression in thyroid tissues from a series of papillary carcinoma cases and normal controls, and (ii) whether there are correlations between tissue ghrelin and obestatin levels in series of papillary carcinoma cases and normal controls. Immunohistochemical analysis showed that in sections of benign human thyroid tissue, anti-ghrelin antibody reacted with intense staining in colloid-filled follicles. In benign thyroid tissues, colloids displayed plentiful dispersion in comparison with papillary microcarcinomas, whereas colloids in malignant thyroid tissues were uncommon. We found markedly lower tissue ghrelin levels in thyroid tissue of patients with papillary carcinomas, compared with normal thyroid tissues (P = 0.001). Immunohistochemical analysis also showed that obestatin in papillary carcinoma stained positively to various degrees. Obestatin tissue levels in papillary carcinomas tended to be slightly higher than those in normal thyroid tissue, but this was not statistically significant (P = 0.29). We also report that thyroid tissue of patients with Hashimoto’s thyroiditis produced ghrelin and obestatin at similar levels as in normal thyroid tissue, even though colloid in Hashimoto’s disease is scarce. We conclude that depressed expression of ghrelin, but not obestatin, is specific to papillary carcinoma, and this difference might constitute a diagnostic tool to differentiate papillary carcinoma from normal thyroid tissue. We currently do not know how these peptides are regulated and what factors are involved in papillary carcinoma, which inhibit the expression of ghrelin but not obestatin. This issue warrants further studies.     

Circ_0137287 suppresses cell tumroigenesis and aerobic glycolysis in papillary thyroid carcinoma through miR-183-5p/PPP2R2A axis

Cytotechnology - Circ_0137287 was found to be decreased in papillary thyroid cancer (PTC) tissues and related to aggressive clinicopathologic characteristics. However, the role and mechanism of...     

MicroRNA-4728 mediated regulation of MAPK oncogenic signaling in papillary thyroid carcinoma

Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer that accounts for 85% of thyroid cancers. MicroRNAs (miRNAs) have been reported to play important roles in the biological processes in cancer. In this study, we analyzed the biological role of miR-4728 in human PTC process in human PTC cell lines in vitro. MiRNA-4728 was observed to down-regulated in human PTC tissues and PTC cell lines. Additionally, miR-4728 inhibited PTC cell proliferation. Further study demonstrated SOS1 was repressed by miR-4728 and overexpression of miR-4728 down-regulated both the mRNA and protein levels of SOS1. Moreover, miR-4728 overexpression also decreased the MAPK signaling activity. These observations suggested that miR-4728 could inhibit the process of human PTC through regulating MAPK signaling pathway. And, appropriate regulation of miR-4728 might be vital to improve human PTC treatment.