LRP16影响宫颈癌Siha细胞对化疗药物的敏感性

目的:探讨抑制LRP16的表达对宫颈癌Siha细胞的化疗药物敏感性的影响。方法:将抑制LRP16表达的小干扰RNA:negativecontrol-si RNA(NC)、si RNA-374(si374)转染入Siha宫颈鳞癌细胞系中,通过顺铂(DDP)和紫杉醇(TAX)的处理后,采用CCK-8检测不同浓度紫杉醇、顺铂作用宫颈癌细胞系Siha48 h后,计算出细胞被抑制一半时顺铂、紫杉醇的药物浓度(IC50);使用Hoechst33342染色观察细胞凋亡,采用流式细胞仪检测顺铂IC50作用Siha细胞48小时后的细胞凋亡情况,紫杉醇IC50作用Siha细胞之后的细胞周期分布情况。结果:CCK-8检测转染的Siha细胞增殖活性受到抑制,Hoechst33342染色观察转染的Siha细胞凋亡明显增加,流式细胞仪检测凋亡显示,si374+顺铂的早期凋亡率22.15±2.24,NC+顺铂12.45±2.72,流式细胞仪检测周期显示G2/M(%),si374+紫杉醇29.94±1.87,NC+紫杉醇17.66±2.32。结论:LRP16基因表达下调之后,抑制Siha细胞的增殖、促进其凋亡,使细胞周期滞留于G2/M期,从而提高Siha细胞的化疗敏感性。     

IQGAP1高表达抑制食管鳞癌细胞对顺铂化疗的敏感性

本文旨在研究含IQ模序的GTP酶激活蛋白1(IQ motif containing GTPase-activating protein 1,IQGAP1)过表达或基因干扰是否影响食管鳞癌细胞对顺铂化疗的敏感性。质粒转染构建IQGAP1高表达和基因干扰的稳定细胞系,并采用Western blot进行鉴定。然后,采用不同浓度(2.5μmol/L、5μmol/L、10μmol/L、20μmol/L、40μmol/L)的顺铂处理细胞,通过3-(4,5-二甲基-2-噻唑)-2,5-二苯基溴化四氮唑噻唑蓝[3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide,MTT]法检测IQGAP1高表达、IQGAP1基因干扰和相应对照细胞的活力,通过4′,6-二脒基-2-苯基吲哚(4′,6-Diamidino-2-phenylindole,DAPI)染色和流式细胞技术检测细胞凋亡率,Western blot检测凋亡相关蛋白的表达。结果显示,IQGAP1高表达和基因干扰的稳定细胞系成功建立。在不同浓度的顺铂处理后,MTT结果表明,IQGAP1...     

汉防己甲素联合顺铂对乳腺癌细胞的作用

目的:汉防己甲素和顺铂联合作用乳腺癌细胞,来提高癌细胞对顺铂的敏感性.方法:运用原子力显微镜对乳腺癌细胞表面的超微结构进行表征;MTr法和流式细胞术检测细胞的生长抑制率和细胞周期变化.结果:顺铂和汉防己甲素分别作用乳腺癌细胞48h IC50值为26.33μmoL/l和5.6μmok/l;联合用药组的IC50值为汉防己甲素2.5μmol/L和顺铂13.32μmol/l,在低浓度的联合用药作用乳腺癌细胞24h细胞膜表面结构被破坏,产生孔洞,作用48h被严重破坏使细胞周期在S比例增加为51.7%±0.30%.结论:提高了癌细胞对抗癌药物的敏感性,联合用药通过改变了细胞膜的结构对癌细胞进行有效杀伤,抑制肿瘤细胞生长.     

食管鳞癌Cyclin D1与细胞增殖关系的研究及意义

目的　探讨食管鳞癌细胞中细胞周期素D1(CyclinD1)表达与细胞增殖的关系及意义。方法　应用免疫组织化学和流式细胞术检测 48例食管鳞癌组织中CyclinD1蛋白表达及DNA倍体、S期细胞比值、G2 /M期细胞比值。结果　 48例食管鳞癌中CyclinD1阳性表达率为 45 8%(2 2 / 48) ;DNA异倍体检出率为 5 0 %(2 4/ 48) ,CyclinD1阳性表达的标本中DNA异倍体的检出率为 6 8 2 %(15 / 2 2 ) ,显著高于CyclinD1阴性表达的标本 (33 3%,9/ 2 7,P <0 0 5 )。CyclinD1表达阳性的肿瘤中细胞周期G2 /M期的比值也明显高于CyclinD1表达阴性的肿瘤 (分别为 5 98± 4 87和 4 12± 2 70 ,P<0 0 5 )。结论　从观察结果推测CyclinD1的表达可以加速肿瘤细胞增殖。分析食管鳞癌CyclinD1、DNA倍体及不同时相的细胞增殖有助于帮助分析和判断病人的预后。     

顺铂对HepG2细胞增殖、细胞周期及肝癌干细胞标志物的影响

目的:研究顺铂对HepG2细胞增、细胞周期及肝癌干细胞标志物(CD133、ICAM-1和ABCG2)的影响。方法:选取HepG2作为研究对象,分别采用MMT比色法、PI染色法及免疫荧光法检测不同浓度顺铂对其增殖、细胞周期、CD133、ICAM-1和ABCG2表达的影响。结果:每个浓度顺铂作用后均可以显著抑制HepG2细胞增殖力(F=12.23,P=0.004);顺铂对HepG2细胞增殖力的抑制作用和浓度可能与时间成正比。0 mg/L组静息期(G0/G1期)细胞比例为(50.25±0.79)%、2 mg/L组G0/G1期细胞比例为(89.24±0.41)%、4 mg/L组G0/G1期细胞比例为(29.54±3.02)%,2 mg/L组和4 mg/L组分别比0 mg/L组显著上升和下降,差异明显有统计学意义(t=6.53、-3.65,均P0.05)。0 mg/L组DNA合成期(S期)细胞比例为(47.13±0.74)%、2 mg/L组S期细胞比例为(5.65±0.42)%、4 mg/L组S期细胞比例为(67.46±3.24)%,2 mg/L组和4 mg/L组分别比0 mg/L组显著下降和上升,差异明显有统计学意义(t=-7.35、3.79,均P0.05)。结果提示2 mg/L组和4 mg/L组顺铂可让HepG2在G0/G1期与S期显著阻滞,差异有统计学意义(P0.01);顺铂处理后,剩余的HepG2细胞的CD133、ICAM-1和ABCG2呈现高表达水平。结论:HepG2细胞系中会有很少部分肝癌干细胞避开了顺铂的杀灭作用,是造成临床上肝癌反复发作的重要因素之一,临床上应予以重视。     

三氧化二砷对鼻咽癌细胞Cx43表达的影响

目的:探讨三氧化二砷(As2O3)抑制鼻咽癌的作用机制。方法:采用流式细胞仪(FCM)、激光扫描共聚焦显微镜(LSCM)和荧光技术,检测人鼻咽癌细胞株(CNE1)经As2O3诱导后细胞连接蛋白43(Cx43)表达的变化。结果:FCM显示,经过浓度为4μmol L的As2O3处理后,其Cx43阳性细胞计数率明显升高,与未经As2O3处理和经2μmol L的As2O3处理的CNE1比较,其差异具有非常显著性意义(p<0.01);LSCM图像观察到,经4μmol LAs2O3处理后,标记Cx43的绿色荧光显著增强,集中分布于细胞膜。结论:较高剂量浓度的As2O3能提高鼻咽癌细胞Cx43的表达率,升高细胞膜Cx43的含量。As2O3抑制鼻咽癌细胞生长的作用机制之一,是通过恢复细胞间隙连接通讯功能来实现的。     

抑制JNK通路对胃癌细胞SGC7901增殖、凋亡、迁移和周期的影响

探讨JNK通路抑制剂SP600125对胃癌细胞SGC7901增殖、凋亡、迁移和周期的影响及其机制。以胃癌细胞SGC7901为研究对象,实验分为空白对照组及药物处理组,采用CCK-8法检测不同浓度及不同作用时间SP600125对SGC7901增殖活性的影响,筛选出最佳作用时间与浓度用于后续实验。通过流式细胞术检测SP600125对SGC7901凋亡和周期的影响。Transwell迁移实验检测其对SGC7901迁移能力的影响。Western blotting检测SP600125作用后各组细胞GM130、JNK、p-JNK、c-jun、cleaved caspase-3、bcl-2、MMP-7蛋白水平的变化。研究表明,与空白对照组相比,10μmol/L、20μmol/L、30μmol/L、40μmol/L、50μmol/L浓度均能使SGC7901增殖活性降低,且在40μmol/L水平作用24 h其增殖抑制率最高(p0.05)。在此水平可使细胞凋亡率明显增加(p0.001)。与空白对照组相比,药物处理组细胞处于G2/M期的比例显著增加(p0.01),处于G0/G1期比例减少(p0.01),S期无明显变化,细胞迁移能力也明显下降(p0.01)。Western blotting显示药物处理组与空白对照组相比,蛋白GM130(p0.01)、JNK(p0.01)、P-JNK(p0.01)、c-jun(p0.01)、BCL-2(p0.01)、MMP-7(p0.05)的表达明显下降,cleaved caspase-3表达升高(p0.01)。以上研究表明JNK通路抑制剂SP600125可抑制胃癌细胞SGC7901增殖活性,促进其凋亡,使其周期阻滞于G2/M期,抑制胃癌细胞迁移能力,这可能与其抑制GM130、c-jun、MMP-7等蛋白的表达有关。     

雌激素受体在人舌鳞癌中的表达及β-雌二醇对其增殖的影响

目的：观察雌激素受体（ER）在人舌鳞癌Tca8113细胞系细胞上的表达,研究β－雌二醇（estrabiol,E2)对培养的舌癌细胞增殖的影响。方法：用免疫细胞化学方法和RT－PCR方法检测雌激素受体在人舌鳞癌细胞上的表达,将β－雌二醇（β－E2）作用于体外培养的人舌鳞癌细胞,测定^3H-TdR掺入量,并用流式细胞仪测定细胞周期。结果：经免疫细胞化学和RT－PCR方法可检测到ER－α和ER－β在人舌鳞癌细胞上均有表达,其中ER－β表哒相对较弱。不同浓度的β－E2可增加^3H-TdR掺入量,并存在着剂量效应。106-6mol/L的β－E2能使人舌鳞癌细胞处于G1期的细胞比例从对照组的76．5％下降至62．3％,而处于S期和G2期的细胞比例从23．5％上升至37．7％,细胞的DNA合成增加,促进细胞的增殖。β－E2对舌癌细胞的促增殖作用可被Tamoxifen阻断。结论：在人舌鳞癌细胞上有雌激素受体的表达,且β－E2在体外能明显促进培养的人舌鳞癌细胞的增殖。     

卡铂通过抑制ERK1/2通路诱导人卵巢癌细胞S和G_1期阻滞

卡铂(carboplatin,CBP)是一种抗肿瘤活性较强的化疗药物,通过诱导细胞周期阻滞抑制肿瘤细胞生长,但其诱导细胞周期阻滞的报告不甚一致.本研究探索卡铂对卵巢癌HO-8910细胞生长及细胞周期进程的影响.MTS结果显示,卡铂以浓度和时间依赖方式抑制卵巢癌HO-8910细胞生长,联合使用ERK1/2通路抑制剂PD98059可使卡铂抗卵巢癌细胞增殖作用增强.采用Giemsa染色法观察到,卡铂与PD98059单用或联用均能致卵巢癌细胞发生明显的形态学变化.流式细胞术检测细胞周期发现,随卡铂浓度的增高,S期阻滞作用增强;抑制ERK1/2通路可拮抗卡铂对HO-8910细胞S期阻滞作用,增加G1期阻滞作用,而对G2/M期细胞影响不明显.Western印迹结果显示,随卡铂浓度的增高,p-ERK1/2、Cdc2(Y15)和p-Cdc2(T161)的表达逐渐升高,Cyclin E1和Cyclin B1的表达逐渐降低;抑制ERK1/2通路可将卡铂上调,p-ERK1/2和p-Cdc2(T161)的作用反转为下调作用,上调Cdc2(Y15)的表达受阻,抑制Cyclin B1的下调作用,促进Cyclin E1的下调作用.本研究结果提示,卡铂通过抑制ERK1/2激活,诱导人卵巢癌HO-8910细胞S和G1期阻滞,抑制卵巢癌细胞生长.     

卡铂通过抑制ERK1/2通路诱导人卵巢癌细胞S和G0/G1期阻滞

卡铂(carboplatin, CBP)是一种抗肿瘤活性较强的化疗药物, 通过诱导细胞周期阻滞抑制肿瘤细胞生长, 但其诱导细胞周期阻滞的报告不甚一致. 本研究探索卡铂对卵巢癌HO-8910细胞生长及细胞周期进程的影响. MTS结果显示, 卡铂以浓度和时间依赖方式抑制卵巢癌HO-8910细胞生长, 联合使用ERK1/2通路抑制剂PD98059可使卡铂抗卵巢癌细胞增殖作用增强. 采用Giemsa染色法观察到, 卡铂与PD98059单用或联用均能致卵巢癌细胞发生明显的形态学变化. 流式细胞术检测细胞周期发现, 随卡铂浓度的增高, S期阻滞作用增强; 抑制ERK1/2通路可拮抗卡铂对HO-8910细胞S期阻滞作用, 增加G1期阻滞作用, 而对G2/M期细胞影响不明显. Western印迹结果显示, 随卡铂浓度的增高, p-ERK1/2、Cdc2(Y15)和p Cdc2(T161)的表达逐渐升高, Cyclin E1和Cyclin B1的表达逐渐降低; 抑制ERK1/2通路可将卡铂上调,p-ERK1/2和p-Cdc2(T161)的作用反转为下调作用, 上调Cdc2(Y15)的表达受阻, 抑制Cyclin B1的下调作用, 促进Cyclin E1的下调作用. 本研究结果提示, 卡铂通过抑制ERK1/2激活, 诱导人卵巢癌HO-8910细胞S和G1期阻滞, 抑制卵巢癌细胞生长.     

食管癌细胞诱导肥大细胞迁移的小鼠模型

目的建立小鼠肥大细胞（mast cell,MC）迁移模型,探讨化疗药物三氧化二砷对人食管癌EC109细胞株生长的杀伤机理。方法利用肥大细胞的特征性蛋白酶抗体及其免疫荧光标记MC和PI标记EC109细胞内DNA;以流式细胞术分析小鼠腹腔液中肥大细胞各亚型的百分率及肿瘤细胞周期变化;使用激光扫描共聚焦显微镜显示肥大细胞内分泌颗粒的分布。并通过组织化学方法,观察各种诱导处理后小鼠肠组织肥大细胞由肠道向腹腔移动的变化。结果①根据流式细胞仪点图分布分析,将小鼠肥大细胞分为：类胰蛋白酶阳性、类糜蛋白酶阴性（MC T）;类糜蛋白酶阳性、类胰蛋白酶阴性（MC C）和类胰蛋白酶阳性、类糜蛋白酶阳性（MC TC）三种亚型,且T型MC明显多余TC型和C型（P〈0.05）;以共聚焦显微镜显示三种亚型的MC均含有丰富的分泌颗粒并分布于细胞膜内侧,为其出芽突起形成储备的状态。②经组织切片观察到诱导处理后小鼠肠组织MC由肠道向腹腔移动,且胰酶对MC的诱导作用大于食管癌细胞和As2O3。③经诱导迁移入腹腔的MC可能与癌细胞周期由S期向G2/M期跨越相关;As2O3能延迟食管癌细胞的G0/G1期,阻碍细胞向S期跨越,从而抑制食管癌细胞的生长。结论食管癌细胞移入小鼠腹腔,主要诱导T型MC参与免疫反应。在生物机体内环境（这里指MC影响）的条件下,As2O3对肿瘤细胞生长的作用主要表现为促使癌细胞周期的G0/G1期向S期跨越延迟,或G2/M期进入细胞分裂的延迟。     

LncRNA MIR31HG通过诱导细胞周期阻滞抑制食管鳞癌细胞增殖活性

本研究探讨lnc RNA MIR31HG对食管鳞癌细胞增殖活性的影响.利用定量PCR检测MIR31HG在食管鳞癌标本及其癌旁组织、人食管上皮细胞系Het-1A和食管鳞癌细胞系Eca-109、EC-1、KYSE30中的表达;采用过表达质粒pc DNA3.1-MIR31HG在食管鳞癌细胞系中过表达MIR31HG;MTT法和SRB法检测细胞增殖率;细胞周期分析试剂盒检测细胞周期进程;Caspase3活性检测试剂盒分析Caspase3活性;PCR和Western blot法检测p53、Caspase3及Bcl-2的m RNA和蛋白质表达水平.结果显示,食管癌组织中MIR31HG表达水平显著低于癌旁组织(P0.05);与Het-1A细胞相比,Eca-109、EC-1、KYSE30细胞中MIR31HG的表达均显著下调(P0.05),提示MIR31HG可能介导食管癌的发生发展.转染pc DNA3.1-MIR31HG可显著上调食管癌细胞中MIR31HG的m RNA表达(P0.01),且MIR31HG过表达可显著抑制食管癌细胞增殖活性(P0.05),减少S期细胞数(P0.05),增加G1期细胞数(P0.05),提示MIR31HG可能通过阻碍细胞周期G1期~S期进程抑制食管癌细胞增殖活性.此外,MIR31HG过表达显著增加Caspase3活性,增加Caspase3和p53的m RNA和蛋白质表达水平,同时抑制Bcl-2 m RNA和蛋白质表达水平.这表明,MIR31HG可通过抑制食管癌细胞的增殖活性阻碍食管癌的发生发展,这可能为食管癌的诊断和治疗提供新策略.     

Cell cycle regulator geminin is dispensable for the proliferation of vascular smooth muscle cells

The proliferation of vascular smooth muscle cells (VSMCs) plays a major role in the pathogenesis of many cardiovascular diseases. Geminin regulates DNA replication and cell cycle progression and plays a key role in the proliferation of cancer cells. We therefore hypothesized that geminin regulates the proliferation of VSMCs. The present study demonstrates that the level of geminin expression was low in quiescent VSMCs (approximately 90% and 10% of cells in the G1 and in S/G2/M phases of the cell cycle, respectively), increased as more cells entered in S/G2/M, and then decreased as cells exited S/G2/M. Further, angiotensin II and norepinephrine stimulated expression of geminin in VSMCs. However, the DNA content, nuclear morphology, percentage of cells at different stages of the cell cycle, and rate of proliferation of VSMCs from which geminin was either depleted or overexpressed were all similar. These findings indicate geminin functions differently in VSMCs than it does in cancer cell lines and that it may provide a target for treating cancers without affecting normal cells.     

Enhanced connexin 43 expression delays intra‐mitoitc duration and cell cycle traverse independently of gap junction channel function

Connexins (Cxs) and gap junction (GJ)‐mediated communication have been linked with the regulation of cell cycle traverse. However, it is not clear whether Cx expression or GJ channel function are the key mediators in this process or at what stage this regulation may occur. We therefore tested the hypothesis that enhanced Cx expression could alter the rate of cell cycle traverse independently of GJ channel function. Sodium butyrate (NaBu) or anti‐arrhythmic peptide (AAP10) were used to enhance Cx expression in HeLa cells stably expressing Cx43 (HeLa‐43) and primary cultures of human fibroblasts (HFF) that predominantly express Cx43. To reduce GJ‐mediated communication, 18‐α‐glycyrrhetinic acid (GA) was used. In HeLa‐43 and HFF cells, NaBu and AAP10 enhanced Cx43 expression and increased channel function, while GA reduced GJ‐mediated communication but did not significantly alter Cx43 expression levels. Timelapse microscopy and flow cytometry of HeLa‐WT (wild‐type, Cx deficient) and HeLa‐43 cells dissected cell cycle traverse and enabled measurements of intra‐mitotic time and determined levels of G1 arrest. Enhanced Cx43 expression increased mitotic durations corresponding with a G1 delay in cell cycle, which was linked to an increase in expression of the cell cycle inhibitor p21^waf1/cip1 in both HeLa‐43 and HFF cells. Reductions in Cx43 channel function did not abrogate these responses, indicating that GJ channel function was not a critical factor in reducing cell proliferation in either cell type. We conclude that enhanced Cx43 expression and not GJ‐mediated communication, is involved in regulating cell cycle traverse. J. Cell. Biochem. 110: 772–782, 2010. © 2010 Wiley‐Liss, Inc.     

Connexin 37 profoundly slows cell cycle progression in rat insulinoma cells

In addition to providing a pathway for intercellular communication, the gap junction-forming proteins, connexins, can serve a growth-suppressive function that is both connexin and cell-type specific. To assess its potential growth-suppressive function, we stably introduced connexin 37 (Cx37) into connexin-deficient, tumorigenic rat insulinoma (Rin) cells under the control of an inducible promoter. Proliferation of these iRin37 cells, when induced to express Cx37, was profoundly slowed: cell cycle time increased from 2 to 9 days. Proliferation and cell cycle time of Rin cells expressing Cx40 or Cx43 did not differ from Cx-deficient Rin cells. Cx37 suppressed Rin cell proliferation irrespective of cell density at the time of induced expression and without causing apoptosis. All phases of the cell cycle were prolonged by Cx37 expression, and progression through the G(1)/S checkpoint was delayed, resulting in accumulation of cells at this point. Serum deprivation augmented the effect of Cx37 to accumulate cells in late G(1). Cx43 expression also affected cell cycle progression of Rin cells, but its effects were opposite to Cx37, with decreases in G(1) and increases in S-phase cells. These effects of Cx43 were also augmented by serum deprivation. Cx-deficient Rin cells were unaffected by serum deprivation. Our results indicate that Cx37 expression suppresses cell proliferation by significantly increasing cell cycle time by extending all phases of the cell cycle and accumulating cells at the G(1)/S checkpoint.     

层粘连蛋白对晚G1期人胃癌BGC-823细胞生长的促进作用

为研究层粘连蛋白（laminin,LN）促进肿瘤细胞生长作用,采用脉冲标记计数有丝分裂百分率(percentage labeling mitosis,PLM)法测得体外培养人胃癌 (BGC 823) 细胞周期时间为41 h,其中G1期时间为24.5 h. 分裂细胞脱离法获取分裂期细胞,继续培养23 h,在细胞运行进入G1晚期时,将其置于LN 0、0.11、0.55、1.10 μmol/L基质上孵育4 h; 细胞荧光光度计检测晚G1期细胞内Ca2+浓度、钙调蛋白、DNA含量. 结果显示,LN与其膜上受体结合后引起细胞内Ca2+浓度、钙调蛋白、DNA含量增加,尤以在0.55 μmol/L LN作用显著（P<0. 001）.蛋白质免疫印迹分析证明,cPKC α呈现表达,提示 LN与其受体结合可增强其细胞cPKC-α的活性;分析G1期细胞周期蛋白E(cyclinE)、细胞周期蛋白依赖性激酶CDK2表达水平,呈现逐渐增强的趋势; LN可诱导c-Myc蛋白呈现高表达,提示 LN与其受体结合增强与细胞增殖密切相关的基因表达;在LN作用前后的BGC 823细胞均未检测到Bax蛋白表达.结果提示,在人胃癌 (BGC 823)细胞G1/S期交界处,层粘连蛋白与其膜上受体结合引起细胞内Ca2+浓度升高,诱导钙调蛋白的释放,其含量增加,增强蛋白激酶C的活化,导致细胞内DNA含量增加、G1/S期细胞周期蛋白与CDK表达增强、诱导原癌基因c-Myc呈持续表达状态,而凋亡基因Bax不表达.     

Tumor-Suppressive Function of miR-139-5p in Esophageal Squamous Cell Carcinoma

Recent studies have demonstrated the possible function of miR-139-5p in tumorigenesis. However, the exact mechanism of miR-139-5p in cancer remains unclear. In this study, the association of miR-139-5p expression with esophageal squamous cell carcinoma (ESCC) was evaluated in 106 pairs of esophageal cancer and adjacent non-cancerous tissue from ESCC patients. The tumor suppressive features of miR-139-5p were measured by evaluating cell proliferation and cell cycle state, migratory activity and invasion capability, as well as apoptosis. Luciferase reporter assay and Western blot analysis were performed to determine the target gene regulated by miR-139-5p. The mRNA level of NR5A2, the target gene of miR-139-5p, was determined in ESCC patients. Results showed that reduced miR-139-5p level was associated with lymph node metastases of ESCC. MiR-139-5p was investigated to induce cell cycle arrest in the G0/G1 phase and to suppress the invasive capability of esophageal carcinoma cells by targeting the 3′UTR of oncogenic NR5A2. Cyclin E1 and MMP9 were confirmed to participate in cell cycle arrest and invasive suppression induced by NR5A2, respectively. Pearson correlation analysis further confirmed the significantly negative correlation between miR-139-5p and NR5A2 expression. The results suggest that miR-139-5p exerts a growth- and invasiveness-suppressing function in human ESCCs, which demonstrates that miR-139-5p is a potential biomarker for early diagnosis and prognosis and is a therapeutic target for ESCC.     

桦木酸对人胃癌MGC-803细胞增殖的影响

目的:探究不同浓度桦木酸对人胃癌MGC-803细胞增殖的影响.方法:将人胃癌MGC-803细胞分成4组,每组设置3个复孔,对照组细胞为加入浓度为0 μg/ml的桦木酸实验组细胞分别加入终浓度为10、20、30 μg/ml的桦木酸,各组细胞在含5％的CO2培养箱中孵育48 h后,使用吉姆萨染色法和台盼蓝拒染法检测桦木酸对...