红参含药血清对人乳腺癌MCF?鄄7细胞增殖和细胞周期的影响

[目的]研究红参含药血清对人乳腺癌MCF-7细胞增殖和细胞周期的影响.[方法]采用MTT法观察红参含药血清对人乳腺癌细胞MCF-7的增殖活性.流式细胞术检测人乳腺癌细胞MCF-7的细胞周期、细胞凋亡率.[结果]红参低剂量含药血清对MCF-7细胞有促增殖作用,24、48、72h时增殖率分别为105.9％、115.9％和121.5％.而高剂量对MCF-7细胞表现为抑制作用.红参低剂量组使MCF-7细胞S期DNA含量比例明显增多,高剂量组使细胞周期阻滞在G0/G1期,并能够诱导细胞凋亡,凋亡率达26.86％.[结论]红参含药血清在高剂量时抑制MCF-7细胞生长,低剂量时对细胞具有促增殖作用.     

稳定表达Cyclin E细胞系的建立及Cyclin E高表达对人乳腺癌MCF 7细胞生长及细胞周期的影响

 目的 观察cyclin E 的高表达对乳腺癌细胞MCF 7 生长及周期的影响。方法 构建cyclin EcDNA真核表达载体并采用lipofectAMINE 转染方法将其导入MCF 7 细胞,获得稳定表达cyclin E的细胞系。通过对细胞生长曲线绘制、3H TdR测定及细胞周期分布等的分析,观察其对细胞生长、增殖的影响。结果 cyclin E的高表达可以使细胞的生长速度加快（ 约为对照1-52 倍） 及DNA 掺入增加（4-2 倍）,G1 S移行加速;pRB的磷酸化形式的增多（3 倍）.结论 cyclin E的高表达可明显影响MCF 7 细胞的生长、增殖,并可能通过pRB 磷酸化,影响细胞周期G1 S期移行而实现其对生长的调节。     

Differential Suppression of Human Cervical Cancer Cell Growth by Adenovirus Delivery of p53 in vitro: Arrest Phase of Cell Cycle Is Dependent on Cell Line

It has been reported that overexpression of wild-type p53 protein induces suppression of tumor cell growth in vivo and in vitro. In this study, we further evaluated the differential effects of p53 delivered in an adenovirus vector on the cell growth, apoptosis and cell cycle progression in cervical cancer cell lines. We constructed a recombinant adenovirus expressing p53 and then delivered this into cervical carcinoma cell lines (CaSki, SiHa, and HeLa, HeLaS3) along with adenovirus expressing β-galactosidase as a negative control. Adenovirus-delivered p53 overexpression resulted in a more significant suppression of cell growth in HPV 18-infected cells (HeLa and HeLaS3) and a lesser suppression in HPV 16-infected cells (CaSki and SiHa). However, no suppression was observed in cells infected with a negative control virus. p53 overexpression also induced apoptosis and cell cycle arrest, as determined by annexin V and propidium iodide staining. In particular, the cell cycle was arrested in the G₂/M phase in CaSki cells. In contrast, cell cycles were arrested in the G₁ phase in HeLa cells, suggesting that the arrest phase is dependent upon the cervical cancer cell line. Taken together, these data support the idea that overexpressed p53 protein plays a differential role in suppressing cervical cancer cell growth through apoptosis and cell cycle arrest in either G₁ or G₂/M phase, depending on the cancer cell line.     

ZM447439对乳腺癌T47D细胞生长和细胞周期的影响

研究Aurora激酶抑制剂ZM447439对体外培养的人乳腺癌细胞T47D生长和细胞周期各时相的影响。方法：采用四甲基偶氮唑盐法测定ZM447439对乳腺癌T47D细胞增殖的影响;克隆形成实验检测ZM447439对T47D细胞增殖的影响;流式细胞术检测ZM447439对乳腺癌T47D细胞周期各时相的影响。Western blot检测ZM447439对Aurora A,p-AuroraA,Histone H3,p-Histone H3以及CyclinB1的影响。结果：不同浓度的ZM447439处理T47D细胞24、48、72h明显抑制T47D细胞增殖,IC50分别为（9.604±0.982）μmol/L、（3.413±0.533）μmol/L、（0.620±0.208）μmol/L;经药物作用24h后,贴壁细胞出现皱缩、变圆、脱落;克隆形成率由（93.00±2.65）%降至0%;流式细胞术显示G0/G1期细胞由（50.50±1.71）%降至（6.30±0.17）%,S期细胞由（32.50±2.70）%降至0%,G2/M期细胞由（17.00±4.39）%升高至（93.70±0.17）%,G2/M期的阻滞呈现剂量依赖性;Western blot显示Aurora A、Histone H3无明显趋势变化,p-AuroraA、p-Histone H3、CyclinB1随着浓度的增加而减少,都呈现一定的剂量依赖性。结论：ZM447439可抑制T47D细胞生长,产生G2/M期阻滞。     

Inhibitory Effects of Nabumetone, a Cyclooxygenase-2 Inhibitor, and Esculetin, a Lipoxygenase Inhibitor, on N-Methyl-N-nitrosourea-induced Mammary Carcinogenesis in Rats

We investigated the modifying effects of nabumetone, a relatively selective cyclooxygenase-2 inhibitor, and esculetin, a lipoxygenase inhibitor, on N -methyl- N -nitrosourea(MNU)-induced mammary carcinogenesis in female Sprague-Dawley rats. A total of 124 rats, 6 weeks old, were divided into 6 groups. At 50 days of age, groups 1, 2, and 3 were treated with MNU (50 mg/kg body weight) by subcutaneous injection. From the age of 8 weeks, groups 2 and 4 were given 0.03% nabumetone in the diet and groups 3 and 5 were given 0.03% esculetin in the diet. All rats were necropsied at the termination (25 weeks after the start of experiment). The incidence and multiplicity of neoplasms in group 2 were significantly smaller than those in group 1 ( P <0.005 and P <0.001, respectively). The incidence of neoplasms in group 3 was also significantly smaller than that in group 1 ( P <0.05). These results indicate that the intake of nabumetone or esculetin during the time corresponding to the post initiation phase has a chemopreventive effect on MNU-induced mammary carcinogenesis in rats.     

乳腺癌组织中c-erbB-2 p53 PCNA及bcl-2蛋白的表达及其临床意义

目的:探讨生物学指标c-erbB-2、p53、PCNA及bcl-2在乳腺癌中的表达与乳腺癌病理生物学行为的关系.方法:应用免疫组织化学方法对56例乳腺癌组织切片c-erbB-2、p53、PCNA及bcl-2的表达进行检测.结果:c-erbB-2表达41.1%,与组织学分级呈正相关,与临床分期、病理类型、患者年龄(≥35岁)、ER、PR受体关系不密切;p53蛋白表达48.2%,与组织学分级、ER、PR受体呈正相关,与患者年龄(≥35岁)、临床分期、病理类型呈负相关;全组PCNA表达100%;bcl-2表达50.0%,与组织学分级、病理类型、ER、PR受体呈负相关,与临床分期呈正相关,与患者年龄(≥35岁)关系不密切.结论:生物学指标c-erbB-2、p53、PCNA及bcl-2应与临床预后因素临床期别、组织学分级等联合应用,提高对乳腺癌预后评价的正确性.     

野生型p53基因对人胆囊癌细胞生长及致瘤性的抑制作用

目的:研究野生型p53(wtp53)基因对人胆囊癌细胞生长及致瘤性的影响.方法:应用免疫细胞化学染色、PCR产物直接测序方法分析细胞系遗传背景,在脂质体介导下将含有wtp53的真核表达质粒pCMV-p53,导入GBC-SD细胞中.用G418筛选,建立转染克隆细胞系.以PCR,RT-PCR和蛋白印迹证实外源p53基因的整合与表达;以细胞生长曲线和集落形成实验反映细胞增殖状况;以裸鼠移植瘤试验检测体内致瘤性的影响.结果:GBC-SD细胞P53蛋白过表达;直接测序发现第5外显子126位密码子存在TAC→AAC的碱基突变.外源p53基因已整合入转染后的GBC-SD细胞并获稳定表达.表达外源wtp53的GBC-SD-wtp53细胞生长速率减慢、集落形成能力下降及裸鼠致瘤性受到显著抑制.结论:野生型p53基因可有效抑制人胆囊癌GBC-SD细胞的体内、外生长.     

5-氮杂胞苷抑制乳腺癌细胞Bcap-37增殖及逆转RASSF1A基因甲基化作用

背景与目的探讨5-氮杂胞苷对人乳腺癌细胞Bcap-37细胞增殖的抑制作用及作用机制。材料与方法不同浓度的5-氮杂胞苷与Bcap-37细胞共培养后,应用细胞计数法检测Bcap-37细胞生长的情况;应用甲基化特异性PCR法(MethylationspecialPCR,MSP)检测5-氮杂胞苷作用前后RASSF1A基因甲基化、非甲基化状态的改变;采用逆转录PCR检测RASSF1A基因的mRNA表达。结果当5-氮杂胞苷大于5.00μmol/L剂量时对细胞生长呈浓度依赖抑制作用(P<0.01);5-氮杂胞苷作用4d后对Bcap-37细胞RASSF1A基因有去甲基化作用;细胞Bcap-37mRNA表达明显增强。结论特异性甲基转移酶抑制剂5-氮杂胞苷能较好地逆转Bcap-37细胞RASSF1A基因异常甲基化,诱导RASSF1A基因的表达,从而抑制肿瘤细胞生长。     

维生素E琥珀酸酯联合阿霉素对乳腺癌细胞株Bcap-37的生长抑制作用

目的检测维生素E琥珀酸酯（VES）联合阿霉素（ADM）对乳腺癌细胞生长抑制作用。方法以VES联合ADM作用于人乳腺癌Bcap-37细胞24h和36h，VES浓度为5、10、20mg／L，ADM的浓度分别为0．25、1、2mg／L。采用MTT法测定对细胞增殖的抑制作用，以流式细胞仪分析药物联合作用前后乳腺癌细胞凋亡率的变化和对细胞表面Fas表达的影响。结果VES联合ADM对乳腺癌Bcap-37细胞具有显著的生长抑制和凋亡诱导作用。流式细胞仪分析细胞周期，Bcap-37细胞的自然凋亡率为0．7％，5mg／L和20mg／LVES作用24h后凋亡率分别为10．1％和19．2％，lmg／L和2mg／LADM作用24h后的凋亡率分别为16．0％和23．3％。5mg／LVES联合1mg／LADM以及20mg／LVES联合2mg／LADM作用24h后的凋亡率分别升高至31．1％和40．7％。VES联合ADM作用24h后Bcap-37细胞表面Fas表达增强。结论VES联合ADM对乳腺癌Bcap-37细胞具有显著的生长抑制作用，其机制可能与细胞表面Fas表达上调有关。     

Evaluation of the Effect of Orlistatorlistat on Expression of OCT4, Nanog,SOX2, and KLF4 Genes in Colorectal Cancer SW40 Cell Line

Background and Objective: Orlistat drug is one of the most criticalanti-obesity drugs that widely used around the world. The aim of this study was evaluation the effect of orlistat on the expression of OCT4, Nanog, SOX2, and KLF4 genes in the colorectal cancer SW40 cell line. Materials and Methods: SW40 cell line was cultured in DMEM medium contained orlistat for 24h, and cell viability was assessed by MTT assay. The fold changes of expression of OCT4, NANOG, KLF4, and SOX2 at mRNA level against β-actin were determined by real-timePCR. Two-sample t-test and one-way ANOVA were used to compare the mean of expression of different genes in different groups and different concentrations; a significant level of 0.05 was considered in all tests. Results: Our results showed a significant difference in cell viability, when different doses of Orlistat were used for 24 hour. concentrations of 25 and 100 μM reduce significantly the expression of OCT4 (p <0.05) and SOX2 (p <0.05) in the treated group in comparison to control (p <0.05). Also, the mRNA expression of KLF4 and Nanog was reduced significantly after treatment of SW40 cell lines was performed with 100 μM doses of Orlistat (p <0.05). Conclusion: It appears that after further studies in animal and human phases, orlistat can be used for the treatment of Colorectal Cancer.     

p53β异构体在rmhTNF联合顺铂抑制胃癌细胞增殖中的作用

目的 探讨p53β异构体在rmhTNF联合顺铂干预人胃癌细胞MKN45和SGC7901生长实验中的生物学功能。方法 不同浓度rmhTNF单独或联合顺铂作用于人胃癌细胞MKN45和SGC7901,应用细胞增殖/毒性检测试剂盒（CCK-8试剂盒）检测抑制率;巢式反转录多聚酶链反应（RT-PCR）检测p53β和bcl-2 mRNA的表达变化情况。结果 rmhTNF单独或联合顺铂（4 μg/ml）作用MKN45细胞24 h,联合组抑制率大于单独组,且随rmhTNF浓度的增加而增加,组间差异有统计学意义（P<0.05）;在SGC7901细胞中,联合组抑制率虽有增加但差异无统计学意义（P>0.05）。rmhTNF单独使用对MKN45细胞中p53β和bcl-2表达无影响,差异无统计学意义（F=0.006,P>0.05;F=1.179, P>0.05）,而与顺铂联合作用可明显上调p53β和下调bcl-2的表达,并且随rmhTNF浓度的增加,p53β逐渐增加,bcl-2逐渐减少,差异有统计学意义（F=18.577,P<0.01;F=169.309, P<0.01）。在SGC7901细胞中未见p53β表达,但bcl-2高表达。rmhTNF和顺铂单独或联合作用时bcl-2虽有降低但差异无统计学意义（F=1.340, P>0.05）。p53β与bcl-2表达呈负相关（r=-0.897, P<0.01）,细胞抑制率与bcl-2的表达呈负相关（r=-0.906, P<0.01）。结论 rmhTNF和顺铂对p53β阳性的胃癌细胞MKN45表现出明显的抑制效应且rmhTNF和顺铂联合作用时可表现出协同抗肿瘤作用,其协同抗肿瘤效应可能是通过p53β调节下游分子bcl-2实现的。     

紫外线照射对乳腺癌细胞NFkB、p53和MDM2的影响

目的　了解NFkB家族蛋白在乳腺癌细胞系的表达及紫外线照射后所引起的变化。方法　用L_15培养液培养并传代 9个乳腺癌细胞系 ,收获细胞 ,对其进行胞浆、胞核蛋白质提取 ,Western印迹法观察NFkB家族蛋白及其抑制物的表达 ;采用 2 0J/m2 剂量紫外线照射细胞 ,继续培养细胞并提取蛋白质进行检测。结果　 9个乳腺癌细胞系p5 0、p65和IkB_α胞浆表达阳性率分别为 :88 9%、5 5 6%、77 8% ,胞核表达阳性率分别为 :66 7%、44 4%、2 2 2 %。紫外线照射后胞核p5 0、p65和IkB_α阳性率分别为 :10 0 %、10 0 %、3 3 3 %。p5 3在乳腺癌细胞表达阳性率为 44 4% ,MDM2表达阳性率为 3 3 3 % ,紫外线照射后p5 3和MDM2表达阳性率分别为 :66 7%、77 8%。结论　NFkB、p5 3和MDM2与乳腺癌细胞的发生、发展有关。紫外线照射可引起胞核NFkB及细胞MDM2阳性率明显提高 ,NFkB和MDM2可望成为判断乳腺癌预后新的标志物。     

一氧化氮对胃癌细胞AGS 生长的抑制及其机制探讨*

目的:探讨外源一氧化氮（nitric oxide,NO）对胃癌AGS 细胞生长及c-jun和c-fos表达的影响。方法:应用MTT 法评价NO供体硝普钠（sodium nitroprusside,SNP ）,SNP 的同源类似物铁氰化钠Na3Fe（CN）6 和一氧化氮合酶（nitric oxide synthase,NOS ）抑制剂N-硝基-L- 精氨酸甲酯（N-nitro-L-arginine methylester ,L-NAME ）对胃癌细胞生长的抑制作用,RT-PCR 和免疫印迹检测c-jun和c-fos的基因和蛋白表达。结果:SNP 剂量依赖性的抑制AGS 细胞的生长,其IC 50值为2.13mmol/L 。1mmol/L SNP 处理12、24、48h 后,细胞生长抑制率分别为（16.12± 0.85）% 、（20.33± 1.31）% 、（22.06± 2.03）%（P<0.05）,NOS 抑制剂L-NAME 预处理明显减弱了SNP 对癌细胞的生长抑制效应,Na3Fe（CN）6 对胃癌细胞生长无抑制。与对照组比较,SNP 使c-jun和c-fos的mRNA 和蛋白表达降低,NOS 抑制剂L-NAME 预处理逆转了SNP 的这种作用,Na3Fe（CN）6 对c-jun和c-fos的mRNA 和蛋白表达无影响。结论:NO可诱导胃癌细胞c-jun和c-fos表达降低,抑制癌细胞生长。      

米非司酮对绒癌细胞体外增殖及对非经典人类白细胞Ⅰ类抗原表达的影响

 目的 探讨米非司酮对绒癌细胞JEG 3体外增殖及对非经典人类白细胞I类抗原HLA G、HLA E表达的影响。方法 体外培养高表达HLA G、HLA E的绒癌细胞株JEG 3，采用MTT法检测米非司酮对细胞增殖的影响，分别通过RT PCR技术和流式细胞分析技术观察其对细胞中HLA G、HLA E mRNA和蛋白水平表达的影响。结果 米非司酮对JEG 3细胞的增殖表现出浓度信赖性的抑制作用，高浓度米非司酮能明显下调JEG 3细胞中HLA G、HLA E mRNA和蛋白水平。结论 米非司酮抗肿瘤的机制之一可能是其可以打破机体对肿瘤的免疫耐受，从而遏制肿瘤的生长。     

野生型p53基因转染对卵巢癌细胞生长及药物敏感性影响

目的：探讨野生型p53基因转染对人卵巢癌细胞株SKOV-3的体外生长及裸鼠体内致瘤性抑制作用。并了解p53基因与SKOV-3细胞对顺铂敏感性之间的关系。方法：利用脂质体介导,将含有人野生型p53cDNA的真核表达质粒pCB6-p53导入SKOV-3细胞中,观察该细胞体外生长和裸鼠体内致瘤性改变;应用流式细胞仪检测细胞周期及凋亡情况,MTT法检测细胞药物敏感性改变。结果：免疫组化法证实外源性p53基因在阳性细胞克隆稳定存在;转染野生型p53基因的SKOV-3细胞体外生长速率下降,裸鼠体内致瘤性丧失;G1/G0期细胞百分比（81.5%)和凋亡细胞百分比（11%）增高;p53表达阳性的SKOV-3细胞对顺铂的敏感性明显增强。结论：野生型p53基因转染能使SKOV-3细胞出现生长抑制和对顺铂的化疗敏感性增强。     

阿司匹林、扑热息痛和尼美舒利对人卵巢癌细胞株SKOV3的抑制作用

[目的]研究非甾体类药物阿司匹林、扑热息痛和尼美舒利对人卵巢癌细胞株SKOV3的抑制作用及其相关机制.[方法]利用四甲基偶氮唑蓝(MTT)法观察阿司匹林、扑热息痛和尼美舒利对人卵巢癌细胞株SKOV3的生长抑制作用;免疫组化法检测COX-2在SKOV3细胞中的表达情况以及3种药物对SKOV3细胞中Ki-67,C-erbB-2表达的影响;透射电镜观察3种药物作用SKOV3细胞后形态变化和凋亡情况;流式细胞术检测3种药物对SKOV3细胞周期的影响.[结果]阿司匹林、扑热息痛和尼美舒利对人卵巢癌细胞株SKOV3具有生长抑制作用,并呈时间-剂量依赖性.免疫组化发现COX-2在SKOV3细胞中呈阳性表达,阿司匹林使SKOV3细胞中C-erbB-2蛋白表达下降,尼美舒利使SKOV3细胞核中Ki-67蛋白表达下降,扑热息痛对C-erbB-2和Ki-67蛋白表达无影响.透射电镜可见阿司匹林、扑热息痛和尼美舒利作用后的SKOV3细胞中有凋亡小体和坏死细胞的形成.流式细胞术发现400μmol/L尼美舒利和10-2mol/L阿司匹林使SKOV3细胞停滞在G0/G1期.[结论]非甾体类药物,特别是COX-2抑制剂尼美舒利可望作为预防性化疗药物应用于卵巢癌的治疗.     

Inhibition of Growth,Induction of Apoptosis and Alteration of GeneExpression by Tea Polyphenols in the Highly Metastatic Human Lung Cancer Cell Line NCI-H460

Lung cancer is a complex group of diseases but each lesion is thought to originate from a single mutated progenitor ‍cell. It is evident that multiple genetic changes are involved in the generation of each specific type of lung cancer. Due ‍to the high complexity of these processes and rapid metastasis, treatment of advanced lung cancer, particularly of ‍NSCLCs, is far from satisfactory. Thus, there is a need for innovative strategies for modulation of adverse alteration ‍in protooncogene or tumor suppressor genes so that lung carcinogenesis can be suppressed or delayed. To this end, ‍we have evaluated the effects of tea compounds (theaflavins, epicatechin-gallate and epigallo-catechin-gallate) on ‍proliferation and apoptosis and associated gene expression in a highly metastatic human lung cancer cell line NCIH460. ‍Significant reduction of cell proliferation, detected in situ by BrdU incorporation, and induction of apoptosis, ‍assessed by the by the TUNEL method, were noted following treatments. Expression of p53, Bcl-2, c-Myc and H-Ras, ‍was localized by immunocytochemistry and analysed by Western blotting. Tea compounds upregulated expression ‍of p53, downregulated expression of Bcl-2 but there was no significant influence on H-ras and c-Myc expressions. It ‍is suggested that tea compounds can influence genetic alteration to disfavour, growth and survival of lung cancer ‍cells.     

The Inhibitory Effect of the Combination of Antineoplaston A-10 Injection with a Small Dose of cis-Diamminedichloroplatinum on Cell and Tumor Growth of Human Hepatocellular Carcinoma

The inhibitory effects of a combination of Antineoplaston A-10 Injection with a small dose of m-diamminedichloroplatinum (CDDP) on cell and tumor growth was tested in in vitro and in vivo settings. A human hepatocellular carcinoma cell line (KIM-1) was used for the cell growth and transplanted tumor growth studies. In the cell growth study, one-hour exposure of KIM-1 cells to CDDP in the medium at concentrations of 0.5, 1.0, and 2.0 μg/ml inhibited cell growth dose-dependently. Continuous exposure of cultured cells to Antineoplaston A-10 Injection at concentrations of 4, 6, and 8 mg/ml also inhibited tumor growth dose-dependently. The combination of 0.5 μg/ml CDDP and 6 mg/ml A-10 Injection inhibited cell growth more than did each agent individually. Electron microscopic study showed well-maintained organelle structures in Antineoplaston A-10 Injection-treated cells compared to CDDP-treated cells. α-Fetoprotein (AFP) production by 10⁴ cells in 48 h increased in the A-10 Injection-treated and A-10 Injection + CDDP-treated groups as the concentration of these agents increased. In the tumor growth study, daily administration of Antineoplaston A-10 Injection 75 mg with once a week administration of 20 μg of CDDP for 5 weeks inhibited transplanted tumor growth in athymic mice after 33 days of treatment, while administration of 75 mg of A-10 Injection or 20 or 60 μg of CDDP alone showed no significant inhibition of tumor growth.     

曲古抑菌素A 对人结肠癌细胞株Colo205 组蛋白乙酰化及ING1b mRNA表达的影响*

目的：探讨曲古抑菌素A（TSA ）对人结肠癌细胞株Colo 205 组蛋白乙酰化及ING 1b mRNA 表达的影响。方法：培养人结肠癌细胞株Colo 205,对照组（A 组）不加TSA 干预,实验组分3 组（B、C、D 组）,分别应用组蛋白去乙酰化酶（HDACs）抑制剂TSA50、100、200 μ g/L 的浓度作用于人结肠癌细胞株Colo 205,24h 后用染色质免疫沉淀（ChIP）方法检测4 组Colo 205 细胞乙酰化组蛋白H3 结合的DNA情况,以了解抑癌基因ING 1b 相关组蛋白H3 乙酰化的变化,并用逆转录聚合酶链反应（RT-PCR）方法检测ING 1b mRNA 的表达,均用实时定量PCR 方法分析。结果：A 组人结肠癌细胞株Colo 205 组蛋白H3 乙酰化水平及ING 1b mRNA Ct值为23.25± 0.08和23.32± 0.05,经TSA 干预后,C、D 组组蛋白H3 乙酰化水平较A 组增加（P<0.05）,2-Δ Δ Ct值分别为4.21和4.38,ING 1b mRNA 表达亦比A 组高（P<0.05）,2-Δ Δ Ct值分别为4.52和4.62,组蛋白H3 乙酰化水平及ING 1b mRNA 表达C、D 组间无显著性差异（P>0.05）,组蛋白H3 乙酰化水平及ING 1b mRNA 表达B 组与A 组比较无显著性差异（P>0.05）,2-Δ Δ Ct值分别为1.12和1.33。同时观察到C、D 组Colo 205 细胞较A、B 组细胞生长明显受抑制。结论：人结肠癌细胞株Colo 205 组蛋白去乙酰化可能是导致基因ING 1b 表达沉默的主要原因之一,100 μ g/L 的TSA 能较好地提高组蛋白乙酰化水平,并有效地激活去乙酰化所致ING 1b 基因转录,诱导该基因表达,从而抑制肿瘤细胞生长。