三氧化二砷对人宫颈癌Hela细胞系的放射增敏作用

目的 探讨三氧化二砷（As2O3）对人宫颈癌Hela细胞系的放射增敏作用。方法 MTT法确定As2O3对Hela细胞的半数致死浓度（LD30），采用集落形成法观察20％该浓度的As2O3对Hela细胞的放射增敏作用。结果（1）细胞生长抑制随As2O3浓度的增加而增强；（2）As2O3＋照射组的细胞存活率低于单纯照射组，耽值小于单纯照射组（1．58Gy、2．11Gy），Dq值也小于单纯照射组（0．27Gv、0．64Gv），存活曲线肩区（Dq）变小，放射增敏比（SER）1．34。结论 As2O3对宫颈癌细胞有明显的放射增敏作用，其作用机理有待进一步研究。     

三氧化二砷对纤维肉瘤细胞放射增敏作用的研究

目的 研究和探讨三氧化二砷（As2O3）是否对纤维肉瘤细胞有放射增敏作用。方法以人纤维肉瘤细胞HTl080为实验对象，首先检测As2O3的单药毒性，确定IC10、IC50和IC90。放射增敏作用的实验分为空白对照组、单纯给药组、单纯照射组（包括1、2、4、6、8、10Gy剂量）、照射前加药组（于照射前24h加入设定浓度的As2O3，药物作用24h后进行照射）和照射后加药组（于照射后即刻加入设定浓度的As2O3，药物作用24h）。所有实验均重复3次。采用克隆形成分析法观察单纯照射和照射联合As2O3对细胞的杀伤作用。计算细胞的存活分数，用多靶单击模型进行拟合并做图。结果 HT1080细胞的IC10、IC50和IC90剂量分别为0．57、3．67和12．0μmol／L。无毒剂量的As2O3照射前给药增敏比（SER）为0．86（Do值比）、0．98（SF2值比），照射后给药SER为0．99（Do值比）、1．09（SF2值比）。IC50剂量的As2O3照射前给药SER为0．90（Do值比）、0．87（SF2值比），照射后给药SER为1．14（Do值比）、1．08（SF2值比）。IC90剂量的As2O3照射前给药和照射后给药的SER均为1．14（Do值比）、3．20（SF2值比），As2O3对低剂量照射的放射增敏作用好于高剂量照射（SERSF2〉SERDo）。结论 As2O3对HT1080纤维肉瘤细胞具有一定的放射增敏作用，为临床放疗和As2O3联合应用提供了实验依据。     

三氧化二砷对人肺腺癌A549细胞的放射增敏作用

[目的]探讨三氧化二砷(As2O3)对人肺腺癌A549细胞的放射增敏作用.[方法]MTT法确定As2O3对A549细胞的半数致死浓度(LD50),采用集落形成法观察20％LD50的As2O3对A549细胞的放射增敏作用.[结果]细胞生长抑制随As2O3浓度的增加而增强.As2O3+照射组的细胞存活率低于单纯照射组,D0值小于单纯照射组(1.46Gy vs 2.03 Gy),Dq值也小于单纯照射组(0.49 Gy vs 1.35Gy),存活曲线肩区(Dq)变小,放射增敏比(SER)为1.39.[结论]As2O3对肺腺癌A549细胞有明显的放射增敏作用,抑制A549细胞的修复能力使照射后细胞存活分数降低是其放射增敏的可能机制.     

盖诺与顺铂联合化疗加同期放射对乳腺癌MCF-7细胞作用的研究

目的：探讨盖诺（NVB）联合顺铂（DDP）的放化同期治疗乳腺癌的有效性、时机选择和作用机制。方法：NVB和DDP（NP方案）对乳腺癌MCF-7细胞联合化疗同期放射。比较照射加联合化疗组和单纯照射组、不同间隔时间联合化放疗的细胞存活率（SF）、凋亡和细胞周期阻滞差异。结果：联合化疗加同期放射后SF较单独放疗更低。化疗处理后间隔4、12和36h照射的SF值最低,0h居中,而阃隔48和72h后,SF值明显上升,放化疗协同杀灭效应减弱,SF最低与最高值相差约15倍。联合化疗加照射组细胞凋亡指数（AI）明显高于单独放射和联舍化疗组。6、8Gy放射后36h时,放化疗联合组与单独放射组比较A1分别高达30．7％、38．35％和2．22％、3．27％,差异有统计学意义,P〈0．05。化疗处理MCF-7细胞1h后在间隔4、12、36和72h处,G2／M周期细胞比例较高,0.48h处较低。结论：联合化放疗对乳腺癌MCF-7细胞具有较强的协同杀灭作用,化放联合治疗的时机选择在肿瘤细胞杀灭过程中具有重要的意义,这种协同杀灭作用与增加细胞凋亡率和化疗造成的细胞G2／M周期阻滞有关。     

DNA-PKcs 表达与鼻咽癌细胞株放射敏感性的关系

 目的 探讨不同放射敏感性鼻咽癌细胞株CNE-1（鼻咽高分化鳞癌细胞株）和CNE-2（鼻咽低分化鳞癌细胞株）中DNA依赖蛋白激酶（DNA-PK）的催化亚基DNA-PKCS基因的表达与鼻咽癌细胞放射敏感性的关系。方法 通过克隆形成实验测定CNE-1、CNE-2不同剂量的存活分数，并用线性二次模型拟合剂量存活曲线求出放射生物学参数α、β,SF2、MID值，以及四氮唑蓝比色分析法（MTT法）检测60Co-γ线4Gy照射后12h细胞的存活率，以评价两株细胞的放射敏感性。逆转录实时荧光定量PCR技术（RTrFQPCR）检测照射前、后不同时间及不同剂量CNE-1、CNE-2细胞mRNA水平DNA-PKCS基因的定量表达。结果CNE-1在各个剂量点的存活分数均比CNE-2高，MID值分别为2．78、1．61，SF2值分别为0．627、0．341；4Gy照射后12h的存活率分别为88．2％、72．3％；RT-FQPCR显示两株细胞中均有DNA-PKCS基因的表达，其相对表达量之比为7．54±2．71（t=4．17，P=0．014），表达差异有统计学意义，DNA-PKCS基因在CNE-2细胞中存在时间、剂量依赖关系。结论实验验证了CNB2比CNE-1对射线更敏感，DNA-PKCS基因的表达与鼻咽癌细胞的放射敏感性有关。     

羟基喜树碱放射增敏作用的离体研究

目的　应用克隆形成方法 ,研究羟基喜树碱 (HCPT)对人鼻咽癌细胞系 (CNE)和胃癌细胞系 (BGC 82 3)的放射增敏作用。方法　实验分为单纯照射组和照射加药组。照射加药组在照射后均立即给予HCPT 2 μg/ml(药物剂量为ID50 剂量 ) ,37℃孵箱内作用 4h。应用克隆形成方法 ,观察单纯照射和照射加HCPT对细胞的杀伤作用。计算细胞存活率 ,用单击多靶数学模型进行曲线拟合做图。结果　BGC 82 3细胞单纯照射组D0 值为 1 17Gy,Dq 值为 1 91Gy,N值为 5 14;照射加HCPT组D0 值为 0 95Gy ,Dq 值为 0 0 1Gy ,N值为 1 0 1;放射增敏比 (SER)为 1 2 3(1 17/ 0 95 )。CNE Ⅰ细胞单纯照射组D0 值为 1 6 0Gy ,Dq 值为 0 6 5Gy ,N值为 1 5 ;照射加HCPT组D0 值为 0 95Gy ,Dq 值为 0 0 1Gy ,N值为 1 0 1;SER为 1 6 8(1 6 / 0 95 )。结论　研究结果显示 ,HCPT具有一定的放射增敏作用 ,为临床的放疗和HCPT的联合应用提供了实验依据。     

汉防己甲素对人肺腺癌细胞的放射增敏作用及其机制的实验研究

目的 探讨汉防己甲素（Tet）对人肺腺癌SPC-A1细胞的放射敏感性的影响及其作用机制。方法 MTT法检测Tet对SPC-A1细胞的增殖抑制作用,比较单纯照射组（4 Gy）、照射（4 Gy）+Tet（1 μmol／L）组、单用Tet组（1 μmol／L）及空白对照组间SPC-A1细胞增殖抑制率的差异。采用克隆形成实验来计算受照射后的细胞存活率,拟合细胞存活曲线,计算D0、Dq、SF2。流式细胞术检测照射前后SPC-A1细胞周期的分布情况。结果 Tet对SPC-A1细胞的24、48和72 h半数抑制浓度（IC50）分别为10.77、5.78、和3.89 μmol／L。照射+Tet组24、48、72 h的细胞增殖抑制率均高于单纯照射组,差异有统计学意义（P＜0.05）。克隆形成实验显示照射+Tet组的D0、Dq和SF2值分别为（1.551±0.045）Gy、（0.522±0.023）Gy和0.503±0.008,均低于单纯照射组。放射增敏比（SER）为1.48。流式细胞仪检测结果显示照射导致了SPC-A1细胞G2期阻滞（P＜0.05）。联合Tet后可以降低G2期阻滞细胞比例（P＜0.05）。结论 Tet可以有效增加人肺腺癌SPC-A1细胞的放射敏感性,其机制可能是通过降低放射导致的G2期阻滞细胞比例,从而使DNA的损伤固定,发生增殖性死亡。     

不同剂量率高能X射线对宫颈癌HeLa细胞生物学效应的影响

目的 观察高能X射线不同剂量率照射对宫颈癌HeLa细胞株克隆形成率、存活率及放射生物学参数的影响。方法 将指数生长期的人宫颈癌HeLa细胞分别采用2、6、10 Gy/min三个剂量率梯度单次照射,照射剂量分别为0、1、2、4、6、8 Gy。照射后置培养箱中继续培养12 d后0.5%结晶紫染色固定,计数大于50个细胞的克隆数。采用GraphPad Prism 5.0软件,根据单靶多击数学模型和线性二次方程（LQ）模型拟合细胞存活曲线,求出三种不同剂量率下HeLa细胞相关放射生物学参数。采用SPSS19.0软件对数据进行统计学分析,组间比较采用随机区组方差分析。结果 （1）HeLa细胞在三种剂量率照射后,对克隆形成率和存活率的影响差异均有统计学意义（P=0.03和0.04）。（2）三种高能X线不同剂量率照射下平均α/β值分别为3.28 Gy、3.35 Gy、3.93 Gy,SF2分别为0.79、0.78 、0.75,三种剂量率对生物学参数α/β、D0、Dq、SF2差异无统计学意义（P>0.05）。结论 高能X射线三种不同剂量率照射HeLa细胞后,随着高能X射线剂量率增大,HeLa细胞存活率趋势逐渐下降,生物学效应逐渐增加。     

己酮可可碱对(E)-(2')-脱氧-氟亚甲基胞苷的放射增敏和细胞周期的影响

目的 观察己酮可可碱（PTX）在体外对（E）－（2’）－脱氧－氟亚甲基胞苷（FMdC)的放射增敏作用和放射引起细胞周期再分布的影响。方法 在人结肠癌细胞系WiDr进行克隆形成分析检测放射增敏效应。常规照射剂量2Gy时的放射增敏比（SERSF2）定义为2Gy时对照组存活分数（SF）和药物处理组SF之比。流式细胞仪应用于分析照射、FMdC和PTX对细胞周期分布的影响。结果 照射前用30mmol/L FMdC处理WiDr细胞48h或照射后立即单用0．5－1．0mmol/L PTX 14d均能观察到各自的放射增敏作用。30mmol/L FMdC和0．25－1．0mmol/L PTX的SERSF2分别为1．09和1．02－1．24。30nmol/L FMdC和0．5mmol/L或1．0mmol/L PTX联合应用时,SERSF2分别增加至1．50和1．66。PTX增强FMdC的放射敏感性。流式细胞仪分析表明,在非同步化WiDr细胞,放射引起G2期阻滞和剂量有关。G2＋M期阻滞在照射后6h可检测,12h达高峰。照射前应用30nmol/L FMdC能够使放射引起的G2＋M期阻滞增多,但PTX能显著去除G2期阻滞。结论 己酮可可增强FMdC放射增敏作用和G2期阻滞去除有关。     

不同剂量电离辐射对大肠癌细胞株HCT-8的多柔比星敏感性的研究

目的研究不同剂量电离辐射作用后多柔比星（阿霉素）对大肠癌多药耐药细胞株HCT-8细胞毒活性的影响,进一步探讨逆转大肠癌多药耐药性的方法.方法体外培养大肠癌细胞株HCT-8,以400 ng/ml阿霉素作为HCT-8细胞耐药模型刺激浓度制备细胞耐药模型.实验模型分为5组：假照射组;大剂量组（2 Gy）;0.05 Gy＋2 Gy组;0.1 Gy＋2 Gy组;0.2 Gy＋2 Gy组.采用MTT法测定给予阿霉素后大肠癌多药耐药细胞株HCT-8的存活率.结果与假照射组相比,2 Gy大剂量照射组及0.2 Gy＋2 Gy组照射后HCT-8细胞存活率明显降低（P＜0.05）,先给予低剂量照射（0.05 Gy,0.1 Gy）后,再给予大剂量照射,HCT-8细胞存活率降低更明显（P＜0.01）.与单纯2 Gy大剂量照射组比较,0.1 Gy＋2 Gy组HCT-8细胞存活率明显降低（P＜0.05）.结论先给予低剂量照射（0.1 Gy）后,再给予大剂量照射,可提高大肠癌多药耐药细胞株HCT-8对阿霉素的敏感性.     

14-3-3 sigma possibly plays a constitutive role in papillary carcinoma, but not in follicular tumor of the thyroid

14-3-3 σ is a negative regulator of the cell cycle and contributes to G2 arrest. Thus far, the lack of its expression due to hypermethylation of the CpG islands has been reported in some carcinomas. In this study, we investigated the expression of 14-3-3 σ in thyroid neoplasms by means of immunohistochemistry as well as Western blot analysis. Normal follicules did not express 14-3-3 σ. In 82 papillary carcinomas, all the cases expressed 14-3-3 σ and its expression was not reduced but even enhanced in the advanced stage and in poorly differentiated types. Furthermore, 21 of the 23 anaplastic carcinomas expressed 14-3-3 σ and its expression level tended to be higher than in papillary carcinoma. On the other hand, none of the 34 follicular carcinomas or 29 follicular adenomas expressed 14-3-3 σ. These results suggest that 14-3-3 σ plays a constitutive role in papillary carcinoma rather than acting as a cell cycle regulator, whereas it is not required for the occurrence and development of follicular tumor.     

Regulation of 14-3-3σ expression in human thyroid carcinoma is epigenetically regulated by aberrant cytosine methylation

Increased 14-3-3sigma expression has been observed by immunohistochemistry in papillary and anaplastic tumors, but not follicular thyroid cancers. 14-3-3sigma mRNA expression and methylation status was examined in tumor cell lines and primary thyroid tissues using real-time RT-PCR, bisulfite sequencing and methylation-specific PCR. Most of the 27 CpG's in the gene's CpG island were methylated in normal thyroid, TPC-1, NPA, FTC-238 and 2-7, which did not express 14-3-3sigma. In contrast, they were unmethylated in KAK-1 and anaplastic lines KAT4 and DRO-90. 14-3-3sigma expression was not increased in thyroid carcinomas, the majority of which had a methylated CpG island. In addition, 5-aza-dC treatment increased 14-3-3sigma expression in the FTC-238 and NPA cell lines, which had low baseline expression. We conclude 14-3-3sigma expression in thyroid carcinomas is regulated by CpG island hypermethylation.     

MRP3／ABCC3的特点及其在肿瘤细胞耐药性方面的作用

化疗是肿瘤综合治疗的主要方法之一，但癌细胞的多药耐药（multidrug resistance，MDR）严重影响患者的化疗效果，耐药癌细胞的存在也是患者术后复发、远处转移直至死亡的根本原因。国内外已经发现了一些MDR相关分子，如P-糖蛋白、多药耐药相关蛋白、谷胱甘肽S转移酶、拓扑异构酶、凋亡相关蛋白等。其中多药耐药相关蛋白3（MRP3／ABCC3）显示了在多种肿瘤细胞包括肺癌中的非小细胞肺癌（non—small cell lung cancer，NSCLC）中与耐药的相关性。     

G3BP和VEGFR-3在大肠癌中的表达及意义

[目的]探讨G3BP和VEGFR-3在大肠癌中的表达及其意义。[方法]选取60例经手术切除癌组织后的大肠癌病人分别选取癌组织和癌旁组织,应用Westernblot方法分别测定G3BP和VEGFR-3在癌组织和癌旁组织中的表达,分析其相关性。[结果]大肠癌组织中G3BP表达的阳性率为70.0%,癌旁组织中未检出G3BP表达;G3BP表达与大肠癌Dukes分期(P<0.05)、淋巴结转移(P<0.05)有显著性相关。大肠癌组织VEGFR-3阳性表达率为58.3%,明显高于癌旁组织VEGFR-3的阳性表达率18.2%(P<0.05);VEGFR-3表达与大肠癌患者的Dukes分期(P<0.05)、淋巴结转移(P<0.05)有显著相关性。G3BP和VEGFR-3在大肠癌组织中表达呈正相关(r=0.376,P<0.05)。[结论]大肠癌中G3BP和VEGFR-3存在明显的高表达,与患者Dukes分期、淋巴结转移关系密切,G3BP和VEGFR-3之间存在显著性相关。     

Interferon-gamma regulation of TNFalpha-induced matrix metalloproteinase 3 expression and migration of human glioma T98G cells

Induction of proinflammatory cytokines in response to malignant cells is an integral component of immune response to control tumor development. However, recent evidences have suggested that tumor cells may evade the immune system and exploit inflammatory responses to enhance its own growth. An exemplary example is the highly invasive and tumor necrosis factor (TNF)alpha-resistant glioblastoma, whose growth is associated with TNFalpha expression. We thus examined whether the tumor takes advantage of TNFalpha overexpression to enhance its invasiveness. To delineate the contribution of inflammation in tumor migration, we demonstrated that the role of proinflammatory cytokines on matrix metalloproteinases-3 (MMP-3) expression, and its consequent effects on the invasiveness of a human glioma cell-line, T98G. By using Matrigel Invasion Chamber, T98G cell migration was significantly enhanced in response to TNFalpha. In contrast, interferon-gamma (IFN gamma) reduced both basal and TNFalpha-enhanced cell invasion. To investigate the mechanisms involved, we demonstrated that TNFalpha upregulated mRNA and protein expression of MMP-3 in T98G cells, whereas IFN gamma downregulated the MMP-3 expression. The role of MMP-3 in glioma invasiveness was further confirmed by transfecting MMP-3 siRNA in T98G to abrogate the TNFalpha-enhanced cell invasion. To delineate the mechanisms further, we showed that IFN gamma exerts an inhibitory effect on the binding of TNFalpha-activated Ets-1 and NF kappa B to their respective enhancer elements found in MMP-3 promoter. In summary, our results indicated that TNFalpha enhances the invasiveness of T98G glioma cells through MMP-3 induction, and such enhancement of cell migration can be inhibited by IFN gamma.     

Predictive value of p53 and 14-3-3sigma for the effect of chemoradiation therapy on esophageal squamous cell carcinoma

BACKGROUND AND OBJECTIVES: The p53 family regulates cell-cycle arrest, triggers apoptosis, repairs DNA damage caused by various genotoxic stresses, and protects cells from death upon irradiation. The purpose of the present study was to examine the expressions of p53 and one of the p53 family proteins, 14-3-3sigma, in biopsy specimens and to predict the clinical and histological responses to chemoradiation therapy (CRT) in patients with esophageal squamous cell carcinoma (ESCC). METHODS: We investigated with the relationship between p53 and 14-3-3sigma expressions in biopsy specimens obtained from 62 patients with ESCC and analyzed these patients' clinical and histological responses to CRT. Chemoradiation therapy consisted of 5-fluorouracil plus cisplatin and 40 Gy of radiation. RESULTS: Following CRT, 71.0% of patients showed a positive clinical response and 52.8% showed a positive histological response. The rate of positive expression was 43.5% for p53 and 58.1% for 14-3-3sigma. Statistically significant correlations were found between p53 expression and clinical response to CRT (P = 0.001) and histological response to CRT (P = 0.041), and between 14-3-3sigma expression and histological response to CRT (P = 0.01). Furthermore, in p53-positive tumors, CRT was more effective in tumors with 14-3-3sigma-positive expressions than those with 14-3-3sigma-negative expressions (P = 0.037). The survival rate of the patients with 14-3-3sigma-positive tumors was better than those with 14-3-3sigma-negative tumors in patients with p53-positive tumors (P = 0.047). CONCLUSIONS: We demonstrated that p53-negative or 14-3-3sigma-positive expressions were closely related to the response to CRT. It is clinically useful to examine the expression of these genes in biopsy specimens for predicting the CRT outcomes in patients with ESCC.     

人肝癌细胞感染蓝舌病毒HbC_3株超微结构的动态观察

目的探讨蓝舌病毒靶向抗肿瘤的细胞生物学机制。方法利用透射电镜观察蓝舌病毒HbC3株感染人肝癌细胞Hep-3B的形态发生学以及该病毒引起的细胞的病理改变。结果BTV-HbC3以受体介导的胞饮作用穿入细胞,溶酶体水解病毒外衣壳,使之成为亚病毒粒子,胞浆内有病毒包涵体及未装配成熟的亚病毒颗粒。随后亚病毒颗粒装配上外层蛋白结构,形成成熟的病毒粒子。病毒感染细胞12~18h时,细胞以挤出的方式释放病毒并达到高峰。18~48h时,病毒进入超感染期,大量细胞发生病变,出现细胞凋亡和溶解。结论一旦蓝舌病毒感染Hep-3B肿瘤细胞即可在细胞内增殖并诱导该肿瘤细胞进入凋亡,死亡的肿瘤细胞释放出的病毒粒子并再次感染其他肿瘤细胞,直至将全部肿瘤细胞杀灭,其溶瘤方式为链式反应。     

IFN-gamma withdrawal after immunotherapy potentiates B16 melanoma invasion and metastasis by intensifying tumor integrin alphavbeta3 signaling

Immunotherapy can effectively suppress tumor, yet complete tumor eradication occurs infrequently. The metastatic potential of remnant tumor cells after immunotherapy and the underlying mechanisms have not been fully elucidated. Here, we report that the termination of immunotherapy strikingly increases the metastatic potential of remnant melanoma. This is mainly due to the withdrawal of IFN-gamma after immunotherapy. The relief of IFN-gamma stress led to the increase of alphavbeta3 integrin expression in B16 cells, which increased the adhesion of B16 cells to fibrinogen, fibronectin and laminin. Through alphavbeta3 signaling, the activation of FAK, upregulation of cdc2, production of active MMP-2 and MMP-9 and actin polymerization were intensified in B16 cells stimulated with ECM molecules 24 h after the withdrawal of IFN-gamma. The i.v. injection of such tumor cells into mice resulted in more metastatic tumor nodes in lung and shortened the survival of mice. The pitfall of immunotherapy termination can be remedied by the administration of recombinant CBD-HepII polypeptide of fibronectin, which effectively inhibits alphavbeta3 signaling. These findings suggest that the risk of tumor metastasis can be increased after the termination of immunotherapy, due to the withdrawal of IFN-gamma and that targeting alphavbeta3 signaling pathway can improve the therapeutic effect of immunotherapeutic approaches by reducing such metastatic risk.     

腹腔热化疗中卵巢癌细胞对顺铂敏感性影响的体外研究

目的:探讨腹腔热疗对卵巢癌细胞顺铂敏感株的化疗增敏作用及对顺铂耐药株的逆转耐药作用,并分析其作用机制,为腹腔热疗增加顺铂化疗敏感性及逆转卵巢癌顺铂耐药提供实验依据。方法:MTT 法研究常温及41℃不同作用时间下温热联合顺铂对卵巢癌细胞敏感株SKOV 3、卵巢癌细胞顺铂耐药株SKOV 3/DDP 的生长抑制作用。Western bloting法检测常温及41℃不同作用时间下ERCC1 基因表达水平。结果:41℃下作用60、90min时对SKOV 3 细胞生长的抑制作用大,差异有显著性,P<0.001。热处理对SKOV 3/DDP 细胞生长有抑制作用,不同时间差异有统计学意义。热疗联合顺铂在常温或41℃下,SKOV 3 细胞对顺铂的敏感性不同,差异有统计学意义（P<0.001）。 且41℃作用90min时敏感性最大（P=0.002）,对顺铂的敏感性提高79.885% 。热处理不同时间,SKOV 3/DDP 细胞对顺铂的敏感性增加,差异有显著性,P<0.001。41℃90min SKOV3/DDP 细胞对顺铂的敏感性提高37.129% 。在SKOV 3 细胞中,ERCC1 表达水平较SKOV 3/DDP 细胞降低,F=32.175,P<0.001。热疗联合顺铂与常温下相比,SKOV 3、SKOV 3/DDP 细胞中ERCC1 基因表达水平差异无统计学意义,F=0.962,P=0.443。结论:热疗对卵巢癌细胞SKOV 3 及其顺铂耐药亚株SKOV 3/DDP 细胞有生长抑制作用;热疗联合顺铂可以增加SKOV 3 细胞对顺铂的敏感性,可以部分逆转SKOV 3/DDP细胞对顺铂的耐药性,且最佳作用时间为41℃90min;ERCC1 表达增加与卵巢癌顺铂耐药有关,但热疗联合顺铂对ERCC1 基因表达水平无明显影响,热疗可能通过其他途径增加肿瘤细胞对顺铂的敏感性。