Ｓｕｒｖｉｖｉｎ在喉鳞癌中的表达及其与肿瘤细胞增殖和凋亡的关系*

目的　分析Ｓｕｒｖｉｖｉｎ在喉鳞癌中的表达及其与肿瘤细胞增殖、凋亡的关系,并探讨其与喉鳞癌临床病理特征之间的关系。方法　应用免疫组化染色技术检测Ｓｕｒｖｉｖｉｎ和Ｋｉ-６７在８６例喉鳞癌组织及３２例正常喉黏膜上皮组织中的表达;ＴＵＮＥＬ法检测喉鳞癌细胞的凋亡情况。结果　Ｓｕｒｖｉｖｉｎ在喉鳞癌组织中阳性表达率为６０.５％,高于正常喉黏膜上皮组织的１２.５％（Ｐ＜０.０５）,Ｓｕｒｖｉｖｉｎ阳性表达率与肿瘤临床分期、病理分级、淋巴结转移有关（Ｐ＜０.０５）;喉鳞癌Ｓｕｒｖｉｖｉｎ阳性组中凋亡指数（ＡＩ）低于阴性组（Ｐ＜０.０５）,增殖指数（ＰＩ）高于阴性组（Ｐ＜０.０５）,且Ｓｕｒｖｉｖｉｎ表达与ＡＩ呈负相关（ｒ＝－０.８３１,Ｐ＜０.０５）,与ＰＩ呈正相关（ｒ＝０.８８３,Ｐ＜０.０５）。结论　Ｓｕｒｖｉｖｉｎ在喉鳞癌中高表达,可能与喉鳞癌细胞的增殖和凋亡均有一定的关联。     

喉鳞状细胞癌中PIN1基因扩增及表达异常

目的：研究PIN1基因在喉癌组织中的表达情况。方法：采用差异PCR、核型分析方法检测喉鳞癌及癌旁对照组织中PIN1基因扩增情况;采用RT-PCR检测同批组织中PIN1 mRNA表达情况;采用免疫组织化学、Western Blot方法检测PIN1蛋白表达情况。结果：与癌旁对照组织相比,40例喉癌组织中有9例（9/40,22.5%）存在PIN1基因扩增,27例（27/40,67.5%）PIN1 mRNA过表达,26例（26/40,65%）PIN1蛋白过表达（P〈0.05）。40例中17例原代培养成功,可制备中期染色体标本,其中3例（3/17,17.65%）存在19号染色体增加。结论：喉鳞状细胞中PIN1基因拷贝数增加,PIN1 mRNA和蛋白质过表达,可能与喉癌发生发展有关。     

蛋白酶体抑制剂联合pshSTAT3对喉癌细胞增殖及凋亡的影响

背景与目的:蛋白酶体抑制剂是一种新型抗肿瘤靶向治疗药物,其作用机制复杂.本研究前期的工作已经证实,蛋白酶体抑制剂可以有效抑制人喉鳞癌Hep-2细胞的增殖并诱导其凋亡,但它同时也诱导了p-STAT3蛋白表达水平的升高.本研究旨在探讨pshSTAT3抑制p-STAT3蛋白表达能否增强蛋白酶体抑制剂MG-132对喉癌细胞的抗肿瘤作用.方法:以Hep-2细胞为实验对象,利用四甲基偶氮唑蓝(MTT)法、流式细胞术(flow cytometry,FCM)检测MG-132单独及联合pshSTAT3时,细胞增殖抑制率及凋亡率的变化;Western印迹法检测各组p-STAT3蛋白表达情况.结果:MTT榆测结果显示,联合组细胞的增殖抑制作用最强,与MG-132组及pshSTAT3组相比较差异均有统计学意义(P＜0.01).FCM检测结果显示,联合组细胞出现明显的凋亡峰,其凋亡率显著高于MG-132组和pshSTAT3组,差异极有统计学意义(P＜0.01).Western印迹法检测结果显示,经2.5μmol/L MG-132处理Hep-2细胞后P-STAT3蛋白表达显著增强;联合组及pshSTAT3组P-STAT3蛋白表达明显减弱.结论:pshSTAT3可以抑制MG-132诱导的p-STAT3蛋白表达,从而提高蛋白酶体抑制剂MG-132对喉癌细胞的抗肿瘤作用.     

MiR-203 is downregulated in laryngeal squamous cell carcinoma and can suppress proliferation and induce apoptosis of tumours

MicroRNAs (miRNAs) have been recognised to regulate cancer development and progression in carcinogenesis as either oncogenes or tumour suppressor genes. However, whether miR-203 plays a crucial role in human laryngeal squamous cell carcinoma (LSCC) remains largely unclear. In the study, we have found that miR-203 expression was significantly lower in LSCC tissues than that in corresponding adjacent non-neoplastic tissues and was negatively correlated with ASAP1 expression level. Lower expression of miR-203 was significantly related to poor differentiation, advanced clinical stages, T3–4 tumour grade, lymph node metastasis and decreased 5-year overall survival. Transfection with miR-203 inhibited proliferation, reduced invasion, induced apoptosis and caused G1 phase cell cycle arrest of Hep-2 cells in vitro, suggesting that miR-203 functioned as a tumour suppressor. We have also tested that over-expression of miR-203 may both suppress the growth of xenograft tumours in mice and downregulate the expressions of ASAP1 in vivo. Furthermore, miR-203 may regulate the expressions of mesenchymal transition (EMT) marker of E-cadherin and cancer stem cells (CSCs) marker of CD44. These findings suggest that miR-203 plays a role as a tumour suppressor in LSCC, likely by regulating ASAP1, probably in relation to EMT and CSCs and may serve as a potential target for therapeutic intervention.     

Tumor suppressor TSLC1 is implicated in cell proliferation, invasion and apoptosis in laryngeal squamous cell carcinoma by regulating Akt signaling pathway

Overwhelming evidence has demonstrated that TSLC1 (tumor suppressor in lung cancer 1), a novel tumor suppressor, is crucially implicated in various biological processes including progression, proliferation and apoptosis during tumorigenesis. However, the exact functions and molecular details of TSLC1 in laryngeal cancer remain ill-defined. Here, the expression of TSLC1 in laryngeal squamous cell carcinoma (LSCC) tissues and cells was detected, and the biological roles of TSLC1 in LSCC cells were investigated. The results showed that expressions of TSLC1 mRNA and protein were significantly reduced in LSCC tissues with low expression in 18 of 85 (21.18?%) and 16 of 85 (18.82?%), respectively. Additionally, statistical analysis revealed a significant correlation of TSLC1 expression with TNM staging and lymph node metastases (P?<?0.05), but not related to age, gender and tumor differentiation (P?>?0.05). Elevation of TSLC1 level inhibited cell proliferation, reduced cell invasion in vitro and induced cell apoptosis in Hep-2 cells, most importantly, TSLC1 upregulation decreased the level of pAkt, but not changed the level of total Akt in Hep-2 cells. Stepwise investigations demonstrated that overexpression of TSLC1 in Hep-2 cells increased caspase-3 activity and expressions of bax and p21 proteins but decreased the levels of bcl-2, MMP-2 and MMP-9 proteins. These data suggest that TSLC1 may exert essential roles in the progression and development of LSCC, and thus TSLC1 may be a potential molecular target for LSCC treatment.     

Hexokinase 2 overexpression promotes the proliferation and survival of laryngeal squamous cell carcinoma

Proliferating cancer cells preferentially use anaerobic glycolysis rather than oxidative phosphorylation for energy production. Hexokinase 2 (HK2) is highly expressed in many malignant cells and is necessary for anaerobic glycolysis. The role of HK2 in laryngeal squamous cell carcinoma (LSCC) is unknown. In this study, the expression of HK2 in LSCC was investigated and the effect of inhibiting HK2 expression with small hairpin RNA (shRNA) on tumor growth was investigated. Using immunohistochemistry, HK2 expression was assessed in LSCC tissues. Human laryngeal carcinoma Hep-2 cells were stably transfected with a plasmid expressing HK2 shRNA (pGenesil-1.1-HK2) and were compared to control cells with respect to the cell cycle, cell viability, apoptosis, and their ability to form xenograft tumors. HK2 expression was significantly higher in LSCC than in papilloma or glottis polypus. Tumor samples of higher T, N, and TNM stage often had stronger HK2 staining. HK2 shRNA reduced HK2 mRNA, protein levels, and HK activity in Hep-2 cells. HK2 cells expressing shRNA demonstrated a higher G0–G1 ratio, increased apoptosis, and reduced viability. Xenograft tumors derived from cells expressing HK2 shRNA were smaller and had lower proliferation than those from untransfected or control-plasmid-transfected cells. In conclusion, depletion of HK2 expression resulted in reduced xenograft tumor development likely by reducing proliferation, altering the cell cycle, reducing cell viability and activating apoptosis. These data suggest that HK2 plays an important role in the development of LSCC and represents a potential therapeutic target for LSCC.     

口腔鳞癌细胞增殖和细胞凋亡的相关性研究

目的：通过观察口腔鳞癌中细胞增殖和细胞凋亡之间的关系,探讨细胞凋亡在口腔鳞癌发生中的作用。方法：利用脱氧核糖核酸末端转移酶介导的dUTP缺口末端标记（TUNEL）技术及增殖细胞核抗原（PC—NA）免疫组织化学染色,对69例（维族36例、汉族33例）口腔鳞癌中的凋亡细胞和增殖细胞进行原位观察和比较。结果：口腔鳞癌不同组织学分级比较,高分化口腔鳞癌与中低分化口腔鳞癌之间增殖指数及凋亡指数均有显著性差异（P〈0．05）,不同部位的口腔鳞癌其增殖指数无显著差异,而舌癌组凋亡指数低于唇癌组和牙龈癌组（P〈0．05）,增殖指数与凋亡指数在口腔鳞癌中呈负相关关系（r=-0．663,P〈0．05）。结论：口腔鳞癌癌变过程不仅存在活跃的细胞增殖,而且存在细胞凋亡之异常,细胞增殖和细胞凋亡平衡失调在舌癌发病中可能起重要作用。     

口腔鳞癌细胞增殖和细胞凋亡的相关性研究

目的:通过观察口腔鳞癌中细胞增殖和细胞凋亡之间的关系,探讨细胞凋亡在口腔鳞癌发生中的作用.方法:利用脱氧核糖核酸末端转移酶介导的dUTP缺口末端标记(TUNEL)技术及增殖细胞核抗原(PCNA)免疫组织化学染色,对69例(维族36例、汉族33例)口腔鳞癌中的凋亡细胞和增殖细胞进行原位观察和比较.结果:口腔鳞癌不同组织学分级比较,高分化口腔鳞癌与中低分化口腔鳞癌之间增殖指数及凋亡指数均有显著性差异(P<0.05),不同部位的口腔鳞癌其增殖指数无显著差异,而舌癌组凋亡指数低于唇癌组和牙龈癌组(P<0.05),增殖指数与凋亡指数在口腔鳞癌中呈负相关关系(r=-0.663,P<0.05).结论:口腔鳞癌癌变过程不仅存在活跃的细胞增殖,而且存在细胞凋亡之异常,细胞增殖和细胞凋亡平衡失调在舌癌发病中可能起重要作用.     

喉鳞癌组织中FHIT表达与细胞增殖、转移的关系

背景与目的:脆性组氨酸三联体(fragilehistidinetriad,FHIT)基因定位于染色体3pl4.2,跨越大多数人类基因组的共同脆性部位FRA3B,为一候选的抑癌基因,在包括头颈部鳞状细胞癌在内的许多人类恶性肿瘤中都存在FHIT基因的异常。本研究的目的为探讨喉鳞癌(laryngealsquamouscellcarcinoma,LSCC)组织中FHIT基因蛋白的表达及其与肿瘤细胞增殖与转移的关系。方法:采用免疫组化S法,检测41例喉鳞癌组织及其相对应的喉切缘非癌组织中FHIT、PCNA的表达。结果:非癌组织和喉鳞癌组织中,FHIT阳性率分别为100%(41/41)和46.3%(1941)(P<0.01)。喉鳞癌中,在TNM分期Ⅰ～Ⅱ期和Ⅲ～Ⅳ期组,FHIT阳性率分别为69.6%和16.7%;淋巴结转移阳性和阴性组分别为20.0%和61.5%。以上两组比较均有显著性差异(P<0.05)。非癌和喉鳞癌组织中,PCNA标记指数分别为(9.98±2.34)%和(50.71±13.64)%,两者有极显著性差异(P<0.01)。喉鳞癌中,FHIT与PCNA表达有明显的负相关关系(P<0.05)。结论:FHIT低表达与喉鳞癌细胞增殖及淋巴结转移有关。     

BMI1 promotes the progression of laryngeal squamous cell carcinoma

BMI1 is highly expressed in several malignant tumors, and its expression level is associated with tumor progression, proliferation, and prognosis. However, no published studies have examined the role of BMI1 in laryngeal squamous cell carcinoma (SCC). Expression of BMI1 in primary tumors was analyzed by immunofluorescence staining, real-time PCR, and Western blotting. BMI1 was knocked down, and proliferation, apoptosis, and cell cycle assays were performed. Sensitivity to radiochemotherapy was evaluated, and tumorigenicity assays were performed in vivo. BMI1 was highly expressed in laryngeal SCCs. BMI1 promoted cell proliferation and tumor progression, and inhibited apoptosis due to influences on the cell cycle. More importantly, BMI1 suppressed the sensitization of laryngeal Hep2 cells to radiochemotherapy. BMI1 is essential to maintain the proliferation and progression of laryngeal SCCs. Therefore, depletion of BMI1 may be a potential therapeutic option for cancer management.     

An activated Notch1 signaling pathway inhibits cell proliferation and induces apoptosis in human esophageal squamous cell carcinoma cell line EC9706

Previous studies have demonstrated that Notch1 signaling pathway plays a major role in maintaining the balance of cell proliferation, differentiation and apoptosis, and is closely associated with tumorigenesis. However, roles of Notch1 signaling pathway in esophageal squamous cell carcinoma (ESCC), which is a common cause of mortality in China, remain poorly understood. Therefore, a novel strategy for seeking a rational molecular therapeutic target for ESCC is urgently needed. The purpose of this study is to examine the effect of the active Notch1 signaling pathway on the proliferation and apoptosis of ESCC cells and to investigate the underlying molecular mechanisms in carcinogenesis of the esophagus. The results revealed that a constitutively activated Notch1 signaling pathway was observed in ESCC cell line EC9706, through a pcNICD vector mediated expression system. Clearly, the activated Notch1 signaling pathway gave rise to proliferation suppression of the cells, accompanied with a cell cycle inhibition at the G0/G1 phase and apoptosis. In contrast to the expression of CDK2, cyclin D1 and cyclin E observed in EC9706 cells untreated and transfected with pcDNA3.1, there was a markedly decrease in the cells stably expressing Notch1 NICD. Up- and down-regulations of GSK3 beta and beta-catenin, respectively, indicated that Notch1 inhibited proliferation and induced apoptosis of EC9706 cells through Wnt-mediated signaling pathway. These findings suggest that Notch1 signaling pathway may participate in carcinogenesis of the esophagus.     

FOXC1蛋白在喉鳞状细胞癌中表达及临床意义

目的：探讨FOXC1蛋白在人喉鳞癌组织中的表达及其与淋巴结转移、分化程度等临床病理参数间的关系。方法：采用免疫组织化学法检测FOXC1蛋白在喉鳞癌（LSCC）及癌旁正常切缘组织中的表达,并结合临床病理学特征进行统计学分析。结果：FOXC1蛋白阳性表达定位于喉鳞癌细胞的胞核或胞浆,其在LSCC组及对照组中的阳性表达率分别为96.8%和27.1%（P〈0.05）,FOXC1浆表达与颈部淋巴结转移、分化程度及分型关系密切,而与性别、年龄、临床分期等无明显关系;FOXC1核表达与分型相关,与其它临床病理学参数间无明显相关。结论：FOXC1蛋白在喉鳞癌组织中阳性表达率明显高于癌旁正常切缘组织,它可能在喉鳞癌的侵袭、转移过程中发挥重要作用。FOXC1可能成为判定喉癌外科切缘及分子靶向治疗的新靶标。     

反义microRNA-21慢病毒表达载体的构建及对喉癌细胞的增殖抑制作用

目的：克隆反义微小RNA hsa-miR-21并构建其慢病毒表达载体,观察反义寡核苷酸重组慢病毒（ASO-miR-21）对喉癌细胞增殖的调控作用。方法：针对hsa-miR-21核苷酸序列,设计并合成mir-21反义寡核苷酸,将pGCSIL-GFP Vector经双酶切后连接产生pGCSIL-GFP-miR-21慢病毒表达载体,PCR筛选阳性克隆,测序鉴定。pGC-LV-miR-21、pHelper 1.0和pHelper 2.0质粒共转染细胞293T,包装慢病毒。以293T细胞绿色荧光蛋白（green fluorescent protein,GFP）的表达水平测定病毒滴度。采用MTT法及克隆形成实验检测反义miR-21（ASO-miR-21）重组慢病毒对喉癌细胞增殖能力的影响。结果：成功构建反义hsa-miR-21的慢病毒表达载体,采用ASO-miR-21抑制喉癌细胞内高水平表达miR-21的活性后,可显著抑制喉癌细胞增殖。结论：成功构建反义miR-21的慢病毒表达载体,ASO-miR-21可以明显抑制喉癌细胞增殖。     

白细胞介素-8沉默对喉鳞状细胞癌细胞增殖和凋亡的影响及机制研究

目的探讨白细胞介素-8(IL-8)沉默对喉鳞状细胞癌细胞增殖和凋亡的影响及相关机制。方法将IL-8小干扰RNA(siRNA)和Lipofectamine 2000转染试剂转染至喉鳞状细胞癌Hep-2细胞作为实验组和NC组仅转染Lipofectamine 2000转染试剂的细胞作为,未做处理的细胞作为空白组。采用噻唑蓝(MTT)法检测细胞增殖能力,流式细胞仪检测细胞凋亡情况,蛋白质印迹法(Western blot)检测IL-8、蛋白激酶B(AKT)、磷酸化AKT(p-AKT)、cleaved caspase 3、B细胞淋巴瘤/白血病-2(Bcl-2)、Bcl-2相关X蛋白(B AX)的相对表达量。结果实验组喉鳞状细胞癌Hep-2细胞中IL-8蛋白的相对表达量明显低于NC组和空白组细胞,OD值明显低于NC组和空白组细胞(P<0.01)。实验组喉鳞状细胞癌Hep-2细胞的凋亡率明显高于空白组和NC组细胞(P<0.01)。实验组Hep-2细胞中p-AKT和抑制凋亡蛋白Bcl-2的相对表达量均低于空白组和NC组细胞,而促凋亡蛋白B AX和cleaved caspase 3的相对表达量均高于空白组和NC组细胞(P<0.05)。3组Hep-2细胞AKT蛋白的相对表达量比较,差异均无统计学意义(P>0.05)。结论IL-8可通过对磷酸肌醇3-激酶(PI3K)/AKT相关信号通路的调控,抑制喉鳞状细胞癌Hep-2细胞的增殖能力,并促进其凋亡,为喉鳞状细胞癌的诊断和治疗提供了新的靶点及可能的治疗策略。     

PSMD7基因在人食管鳞癌组织中的表达及影响癌细胞增殖、凋亡的机制研究

背景与目的：26S蛋白酶体非ATP酶调节亚基7（26S proteasome non-ATPase regulatory subunit 7,PSMD7）作为组成19S蛋白酶体盖子结构的核心成员是否参与肿瘤的发生、发展,以及具体的分子机制尚不清楚。本实验将研究PSMD7基因在人食管鳞癌组织中的表达,以及对癌细胞增殖及凋亡的影响。方法：采用实时荧光定量聚合酶链反应（real-time fluorescent quantitative polymerase chain reaction,RTFQ-PCR）和蛋白质印迹法（Western blot）检测食管鳞癌及其癌旁正常组织标本中PSMD7的mRNA及蛋白表达情况。在人食管鳞癌细胞系TE-1中,用慢病毒介导的RNA干扰技术下调PSMD7的表达,观察细胞增殖及凋亡的变化,检测线粒体膜电位的变化、细胞质中Cyt C的表达以及凋亡相关因子的表达。结果：PSMD7基因的mRNA和蛋白在食管鳞癌组织中的表达显著高于癌旁正常组织（P<0.05）,PSMD7蛋白的高表达与淋巴结转移阳性呈正相关（P<0.05）。抑制PSMD7蛋白的表达可使细胞的增殖能力降低（P<0.05）,并促进细胞的凋亡（P<0.05）,同时线粒体膜电位降低,促进Cyt C释放进入细胞质,激活caspase级联反应,说明抑制PSMD7的表达诱导细胞凋亡是通过线粒体信号通路进行的。结论：PSMD7在食管鳞癌中呈高表达,并通过线粒体依赖的方式促进TE-1细胞凋亡。     

Distant metastases in laryngeal squamous cell carcinoma

Distant metastases (DM) is the point of concern and seems to be on the rise with the improved control of the laryngeal cancer in the primary site and neck regions. Prognostic factors must be evaluated to improve the detection of DM at early stage of the disease. Therefore, we have analyzed our cases of laryngeal squamous cell carcinoma with DM to find out the risk factors in these patients. We analyzed the records of laryngeal squamous cell carcinoma patients with DM. The records were evaluated according to distant metastases site, TNM staging, the metastases at the neck, treatment and survival. The incidence of DM was 7.2% in our series. Lung is the most common site of DM in laryngeal squamous cell carcinoma. Staging grouping has been helpful in predicting DM, most of the cases were in stage III and IV (85%). Supraglottic lesions is the most common site in patients with DM. The recurrence in the locoregional site was observed in 47% of cases. The overall survival with DM is 28 months, without DM 22 months. The patients with DM in laryngeal squamous cell carcinoma were from the group with supraglottic lesions, stage 3, 4a and 4b. Stage grouping seems to be a better indicator of DM rather than T or N stage alone. The most common site of metastasis is the lung.     

抑癌基因PTEN/MMAC1/TEP1在肾癌组织中的表达及其与细胞增殖和凋亡的关系

背景与目的:PTEN/MMAC1/TEP1是近来新发现的具有磷酸酯酶活性的抑癌基因,有研究证实PTEN在人类多种肿瘤中存在丢失或突变,与肿瘤的发生、发展密切相关,但在肾癌中研究较少。本研究拟探讨肾细胞癌(renalcellcarcinoma,RCC)中抑癌基因PTEN的蛋白表达及其与肾癌生物学行为的关系。方法:收集44例手术后并经病理学检查证实的RCC组织、15例癌旁非癌肾组织及10例非瘤正常肾组织,采用免疫组化SP法进行PTEN蛋白检测,按PTEN蛋白阴、阳性各选15例RCC组织和10例正常肾组织,用流式细胞仪检测细胞的增殖指数和凋亡率,从而分析PTEN蛋白与肾细胞增殖和凋亡的关系。结果:PTEN蛋白在肾组织中表达主要位于胞浆,RCC组织中PTEN阳性表达率为36.36%,显著低于癌旁非癌肾组织(73.33%)及正常肾组织(100%)(P<0.01),在不同组织类型中无统计学差异(P>0.05)。PTEN蛋白在Ⅰ、Ⅱ期RCC组织中表达显著高于Ⅲ、Ⅳ期RCC组织(P<0.05),PTEN蛋白阳性RCC细胞的增殖指数为(5.6±0.8)%,显著低于PTEN蛋白阴性者的(15.6±1.6)%(P<0.01),而PTEN蛋白阳性者的细胞凋亡率为(6.5±1.9)%,显著高于PTEN蛋白阴性者的(2.8±1.6)%(P<0.01)。结论:PTEN蛋白在RCC组织中的阳性表达明显下降,其抑癌作用机制可能是诱导细胞周期阻滞在G1期和增加细胞凋亡率,提示检测PT     

食管鳞癌组织AIB1与Ki-67表达相关性研究

目的:探讨食管鳞癌组织AIB1的表达水平及其与Ki-67的相关性.方法:用免疫组织化学SP方法,联合检测20例正常食管鳞状上皮组织和60例食管鳞癌组织中AIB1和Ki-67的表达,分析AIB1的表达与临床病理参数的关系以及与Ki-67的相关性.结果:20例正常食管鳞状上皮组织中呈微弱表达或不表达,60例食管鳞癌组织中有25例(41.6％)为AIB1高表达,P＜0.05.AIB1的表达水平与临床分期、淋巴结转移有明显相关性;在T3～T4期的表达水平高于T1～T2期(P＜0.05),在有淋巴结转移的组织中表达较高(P＜0.05),而其在不同性别、年龄、病理学分型中的表达差异无统计学意义,P＞0.05;Ki-67蛋白在食管鳞状细胞癌中的表达为65.0％(39/60),在39例Ki-67蛋白阳性表达的食管鳞癌组织中有29例同时表达AIB1,且其中25例AIB1过表达,AIB1与Ki-67的表达呈中度正相关,P＜0.01.结论:AIB1蛋白与食管鳞癌的临床分期和淋巴结转移有相关性,Ki-67可能也是AIB1蛋白非类固醇激素受体途径的相关蛋白之一.     

Crocin inhibits proliferation and nucleic acid synthesis and induces apoptosis in the human tongue squamous cell carcinoma cell line Tca8113

Background: Cancer chemoprevention is a proven effective strategy for oral squamous cell carcinomas (OSCCs). The present study was designed to investigate the effects of crocin, a potential chemopreventive agent, on growth and DNA and RNA content in a human tongue squamous cell carcinoma cell line, Tca8113. Methods: Tca8113 cells were treated with crocin for 24, 48, 72, and 96 h at concentrations of 0.1, 0.2, 0.4, and 0.8 mM. Tumor cell viability was investigated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. In addition, Tca8113 cells were treated with 0.4 mM crocin and cytotoxic effects as an inducer of apoptosis were analyzed using flow cytometry. Furthermore, acridine orange (AO) staining and observation using laser scanning confocal microscopy (LSCM) were used to determine the effects of the drug on nucleic acid synthesis. Results: Crocin decreased Tca8113 cell viability and growth remarkably at 24, 48, 72, and 96 h, in a concentration-dependent manner (P<0.05). In addition, 0.4 mM crocin significantly induced both early and late apoptosis of Tca8113 cells. Moreover, the cellular DNA and RNA content was significantly downregulated by 0.4 mM crocin compared with the negative control (P<0.01). Conclusions: Our observations support the feasibility of applying crocin as a chemoprophylactic agent and treatment for OSCCs.