益气解毒复方中药对人胃癌移植瘤裸鼠肿瘤生长及胃癌组织Ki-67表达影响的实验研究

目的:探讨益气解毒复方中药对SGC-7901荷瘤裸鼠的抑瘤作用及对肿瘤组织Ki-67表达的影响,为其临床应用提供实验依据.方法:胃癌细胞株SGC-7901接种于裸鼠右后肢皮下.对照组灌胃生理盐水10 mL/kg,5-FU组肌肉注射30 mg/kg,益气解毒复方中药大、中、小剂量组分别灌胃1 500、750和375 mg/mL的药液,各组连续给药14 d,各鼠脱臼处死,计算瘤质量系数,肿瘤组织用于免疫组织化学染色检测肿瘤组织Ki-67表达.结果:对照组的瘤质量系数为3.060±2.426,显著高于5-FU组和益气解毒复方中药大、中剂量组(0.273±0.146,P<0.01;0.696±0.585, P<0.01;1.197±1.271,P<0.05),与益气解毒复方中药小剂量组(1.727±1.721)相比差异无统计学意义,P>0.05.免疫组织化学结果显示,5-FU组、中剂量的益气解毒复方中药组的肿瘤组织Ki-67过度表达率(36.8±10.3)%,(32.5±20.4)%显著低于对照组(59.5±13.9)%,P<0.05.结论:益气解毒复方中药对胃癌细胞增殖和Ki-67表达具有较好的抑制作用.     

吉西他滨抑制骨肉瘤细胞系MG-63增殖和诱导凋亡的实验研究

目的研究吉西他滨对骨肉瘤细胞系MG-63的增殖抑制和凋亡诱导作用。方法利用光镜检测吉西他滨作用后MG-63的形态学变化;MTT法检测吉西他滨对MG-63的增殖抑制;流式细胞仪AnnexinV-FITC法检测细胞凋亡,琼脂糖凝胶电泳检测DNA ladder。结果吉西他滨可明显地抑制MG-63细胞生长,各实验组24、48、72小时抑制率随时间的增加而增加,差异有统计学意义（P〈0.05）,0.1 mg/L及以上浓度的吉西他滨对MG-63骨肉瘤细胞的抑制率可达50%,0.1-100 mg/L的吉西他滨对MG-63的抑制率相似。吉西他滨可诱导MG-63细胞凋亡,在不同浓度吉西他滨（0.1,1.0,10.0,100 mg/L）作用48小时后,MG-63的凋亡率差异无统计学意义（P〉0.05）。并且经琼脂糖凝胶电泳可以显示DNA ladder。结论吉西他滨对骨肉瘤细胞系MG-63具有增殖抑制作用,并且各实验组24、48、72小时抑制率随时间的增加而增加;吉西他滨对骨肉瘤细胞系MG-63具有诱导凋亡作用;0.1-100 mg/L吉西他滨对MG-63的增殖抑制和诱导凋亡作用相似。     

青蒿素对人胃癌裸鼠移植瘤的生长抑制作用及其机制的研究

目的:研究青蒿素对人胃癌细胞株SGC-7901裸鼠皮下移植瘤的生长抑制作用及其机制.方法:建立人胃癌裸鼠皮下移植瘤模型,随机分为实验组即青蒿素低剂量组、青蒿素中剂量组和青蒿素高剂量组、空白对照生理盐水组及阳性对照5-FU组,每组5只,分剐灌胃连续给药10 d,停药后24 h处死裸鼠,称取瘤质量.计算抑瘤率,流式细胞仪检测凋亡率,酶标仪检测Caspase-3的活性变化.结果:高、中、低剂量青蒿素组及5一FU组抑瘤率分别为 71.4%、47.7%、31.3%及45.2%,与生理盐水组比较差异均有统计学意义P<0.05,青蒿素各实验组抑瘤率与5-FU组相比,高、中剂量组明显比5-FU组强,差异有统计学意义,P<0.05.高、中、低剂量青蒿素组及5-FU组流式细胞仪检测时均出现明显的凋亡分布,凋亡率分别为78.0%、65.9%、45.9%和57.9%,酶标仪检测Caspase-3活性发现随着青蒿素剂量的增加Caspase-3活性逐渐增加,其中高剂量青蒿素活性增加最显著.结论:青蒿素对人胃癌细胞株SGC-7901裸鼠皮下移植瘤有明显的抑制作用,在体内可通过活化Caspase-3诱导细胞凋亡而发挥抗肿瘤作用.     

三氧化二砷诱导人膀胱癌T24细胞凋亡的实验研究

目的探讨三氧化二砷(As2O3)诱导人移行细胞膀胱癌细胞株T24细胞凋亡的作用。方法用MTT法、TUNEL法、透射电镜、琼脂糖凝胶电泳等方法观察As2O3诱导T24细胞凋亡的作用。结果As2O3可有效地抑制T24细胞增殖,随着药物浓度增高其抑制作用增强,且细胞出现典型的凋亡变化。DNA琼脂糖凝胶电泳出现凋亡特征性梯形条带。TUNEL法呈阳性结果。透射电镜下可见细胞核仁消失,染色质浓缩聚集于核膜下。对照组均未见上述变化。对凋亡相关基因Bcl-2免疫组化染色发现其表达下调,同时凋亡主要效应分子Caspase 3被激活。结论As2O3可有效诱导膀胱癌细胞凋亡,通过下调Bcl-2基因表达是其作用机制之一。     

天花粉蛋白抑制人乳腺癌MDA-MB-231细胞生长及逆转syk基因甲基化的研究

目的:研究天花粉蛋白(trichosanthin,TCS)抑制人乳腺癌MDA-MB-231细胞增殖和诱导细胞凋亡过程中脾酪氨酸激酶(spleen tyrosine kinase,syk)基因甲基化状态的改变,以寻找新的去甲基化药物.方法:采用MTT法分析TCS对MDA-MB-231细胞增殖的影响,Giemsa染色法观察TCS作用后细胞形态学的变化,FCM检测不同浓度TCS作用48 h后MDA-MB-231细胞凋亡和细胞周期分布情况,甲基化特异性PCR(methylation-specific PCR,MSP)法检测MDA-MB-231细胞经TCS作用前后syk基因甲基化状态的改变,RT-PCR方法分析TCS作用后MDA-MB-231细胞中syk、Dnmts和MBD2 mRNA表达量的变化,比色法检测TCS对MDA-MB-231细胞DNA甲基转移酶活性的影响.结果:TCS体外对MDA-MB-231细胞增殖具有显著抑制作用(P<0.05),并呈时间和浓度依赖性;TCS可诱导MDA-MB-231细胞出现空泡样变性、核固缩和核碎裂等细胞凋亡形态学改变,能使MDA-MB-231细胞凋亡并可诱导细胞生长周期阻滞,凋亡率明显高于对照组(P<0.05),并呈时间和浓度依赖性.TCS可以逆转MDA-MB-231细胞syk基因启动子区甲基化状况;MDA-MB-231细胞syk mRNA表达阴性,经TCS作用后,syk mRNA表达阳性;MDA-MB-231细胞经TCS作用48 h前后Dnmts和MBD2 mRNA表达量没有明显变化(P>0.05),但Dnmts活性降低.结论:TCS在抑制MDA-MB-231细胞增殖、诱导细胞凋亡过程中对syk基因具有明显的去甲基化作用,因而可能成为新型的去甲基化药物.     

地塞米松诱导结肠癌细胞凋亡的实验研究

目的:研究糖皮质激素受体(GR)在结肠癌细胞株Lovo、HCT-116、HT-29和SW-480中的表达,观察地塞米松(Dex)在体外对结肠癌细胞株的增殖抑制和凋亡诱导作用。方法:采用免疫组化、RT-PCR检测糖皮质激素受体(GR)在结肠癌细胞株中的表达;MTT、DNALadder和流式细胞仪等方法进行增殖抑制和细胞凋亡检测。结果:在4种结肠癌细胞株中只有Lovo和HCT-116表达GR。地塞米松在体外作用后,对4种细胞的增殖均有抑制作用,其中对Lovo和HCT-116细胞作用最显著。在Lovo细胞可检测到特征性的凋亡细胞DNA梯带。在流式细胞仪检测显示经1×10-4mol/LDex诱导72h后,在Lovo和HCT-116细胞检测到细胞凋亡,分别为(34.8±1.9)%和(33.6±1.4)%,明显高于未加Dex对照组的Lovo(2.9±0.4)%和HCT-116(6.4±1.3)%,差异有统计学意义(t值分别为28.934和22.980,P值均为0.000)。结论:结肠癌细胞株Lovo和HCT-116表达GR,地塞米松体外抑制Lovo和HCT-116细胞增殖,并诱导其发生凋亡,可能与GR相关。     

植物多酚类化合物抑制人乳腺癌MCF-7/ADM细胞的筛选

目的研究从儿茶素、槲皮素、大豆苷元、芝麻素、阿魏酸和白藜芦醇等六种植物多酚类化合物,筛选出对人乳腺癌MCF-7/ADM细胞具有抑制作用的药物。方法MTT法初筛对MCF-7/ADM细胞具有毒性作用的植物多酚类化合物;再通过均匀设计筛出无毒性剂量时联合多柔比星（阿霉素）对MCF-7/ADM细胞抑制作用最强的植物多酚类化合物;最后经单细胞凝胶电泳检测筛出后的植物多酚类化合物联合阿霉素对正常肝细胞的毒性作用。结果槲皮素、白藜芦醇、阿魏酸能抑制MCF-7/ADM细胞增殖;经均匀设计后认为白藜芦醇联合阿霉素对MCF-7/ADM细胞的抑制作用比其余两者明显;单细胞凝胶电泳试验证明白藜芦醇联合阿霉素对正常肝细胞无毒性作用。结论白藜芦醇联合阿霉素对人乳腺癌MCF-7/ADM细胞具有抑制作用,且基本无毒害作用。     

瘦素对乳腺癌生长细胞动力学和形态学影响的研究

目的：研究瘦素对乳腺癌细胞株MCF-7细胞生长的作用。方法：分别使用0、25、50、100和200nmol／L瘦素作用于细胞株MCF-7细胞，同时在上述作用后24、48和72h采用光学显微镜观察细胞形态学改变，采用MTT比色方法，观察不同浓度瘦素对MCF-7细胞生长刺激的剂量、时间效应，比较在相对应剂量胰岛素情况下，二者对细胞增殖刺激作用的强弱。结果：加用瘦素各组细胞比未加瘦素细胞密度增加，形态变异。与正常对照组相比，各浓度瘦素（25、50、100和200nmol／L）均可明显促进MCF-7细胞增殖，其中50、100和200nmol／L瘦素作用24、48和72h后差异均有统计学意义，P〈0．05。瘦素对MCF-7细胞的增殖作用呈现一定的时间和剂量依赖效应。胰岛素各相对应组之间与瘦素比较，细胞增殖刺激作用差异无统计学意义，P〉0．05。结论：瘦素对乳腺癌细胞株MCF-7细胞增殖有刺激作用，且这种作用呈现一定的剂量、时间依赖效应，结果提示瘦素是促进乳腺癌细胞增殖的因素之一。     

维生素E琥珀酸酯联合他莫昔芬抑制乳腺癌细胞增殖

目的:检测维生素E琥珀酸酯(VES)联合他莫昔芬(tamoxifen)对乳腺癌细胞增殖的抑制作用,并分析调控Fas/FasL系统表达在抑制乳腺癌细胞增殖中的作用。方法:人乳腺癌细胞MCF-7(ER阳性)和MDA-MB-435(ER阴性)以VES联合他莫昔芬作用24和48 h,VES浓度为10和20μg/mL,他莫昔芬的浓度分别为1、5和10μmol/L。以MTT法测定对细胞增殖的抑制作用,以流式细胞仪分析细胞周期和细胞表面Fas/FasL表达的变化。结果:VES联合他莫昔芬对乳腺癌细胞具有显著的抑制作用。药物联合作用后,乳腺癌细胞表现为明显的G0/G1期阻滞,MCF-7和MDA-MB-435细胞的凋亡率分别由(3.30±0.2)%和(4.88±0.9)%升高至(25.61±2.7)%和(23.33±1.1)%,流式细胞仪提示,MCF-7和MDA-MB-435细胞表面的Fas分别由50.07和46.29升高至116.72和136.68;FasL分别由51.85和57.43升高至146.82和127.90。结论:VES联合他莫昔芬对乳腺癌细胞具有显著的抑制作用,其机制可能与细胞表面Fas和FasL表达上调有关。     

Suppressing NRIP1 inhibits growth of breast cancer cells in vitro and in vivo

Earlier age at menarche is a major risk factor for breast cancer. Our previous study identified Nrip1 (also known as Rip140) as a candidate gene for delaying female sexual maturation (FSM) and found that knocking out Nrip1 could significantly delay FSM in mice. To investigate the effects of NRIP1 in breast cancer we used human cell lines and tissue arrays along with an in vivo study of DMBA-induced carcinogenesis in Nrip1 knockout mice. Analysis of tissue arrays found that NRIP1 is elevated in tumors compared to cancer adjacent normal tissue. Interestingly, in benign tumors NRIP1 levels are higher in the cytosol of stromal cells, but NRIP1 levels are higher in the nuclei of epithelial cells in malignancies. We also found overexpression of NRIP1 in breast cancer cell lines, and that suppression of NRIP1 by siRNA in these cells significantly induced apoptosis and inhibited cell growth. Furthermore, in vivo data suggests that NRIP1 is upregulated in DMBA-induced breast cancer. Importantly, we found that DMBA-induced carcinogenesis is suppressed in Nrip1 knockdown mice. These findings suggest that NRIP1 plays a critical role in promoting the progression and development of breast cancer and that it may be a potential therapeutic target for the new breast cancer treatments.     

Re-activation of the p53 pathway inhibits in vivo and in vitro growth of hormone-dependent human breast cancer cells

Mutations in wild-type p53 (wtp53) protein lead to loss of its tumor suppressor function in breast cancer cells, facilitating uncontrolled tumor growth. Consequently, procedures to repair defective p53 functions in tumor cells are being actively pursued. We sought to determine whether expression of wtp53 protein, or conversion of endogenous mutant p53 (mtp53) into a functional p53 protein with small molecule PRIMA-1, can override the tumor-promoting effects of naturally occurring mtp53 protein in hormone-responsive T47-D human breast cancer cells. We show that transfection of wtp53 gene into T47-D cells suppresses their proliferation in regular media, and inhibits estrogen-dependent cell proliferation in media containing dextran-coated charcoal treated serum. Growth inhibition was not due to the absence of estrogen receptor-alpha or estrogen receptor-beta though receptor levels for estrogen receptor-alpha were drastically reduced in wtp53 expressing cells. Focused microarray analysis of wtp53 expressing cells revealed suppression of PCNA cell-cycle regulatory mRNA and protein. Wild-type p53 transfected T47-D cells also failed to grow in vivo in estrogen supplemented nude mice. Furthermore, xenografts obtained with parental T47-D cells expressing mtp53 grew poorly in nude mice treated with PRIMA-1. PRIMA-1 treated tumors exhibited a low proliferation index, even though mice were estrogen-supplemented. PRIMA-1 treatment of tumor cells suppressed VEGF and induced expression of estrogen receptor-beta though expression of estrogen receptor-alpha and progesterone receptors was unaffected. These data indicate that alteration of the p53 signal transduction pathway by re-expression of wtp53 protein in T47-D cells, or treatment of parental cells with PRIMA-1, can prevent in vivo and in vitro proliferation of T47-D breast cancer cells.     

Targeting highly expressed extracellular HSP90 in breast cancer stem cells inhibits tumor growth in vitro and in vivo

Breast cancer stem cells (BCSC) have been identified in breast carcinoma as CD44⁺/CD24^?/low cells, which display tumorigenic activity and have the ability to self-renew, differentiate and metastasize. Previous studies showed that extracellular HSP90 (eHSP90) participates in the invasion and metastatic processes of various cancers including breast cancer. Here, we show for the first time that eHSP90 is over-expressed in mammosphere cultures that are derived from the MDA-MB-231, MDA-MB-453 and MCF-7 breast cancer cell lines. These mammospheres are highly enriched in cells of the CD44⁺/CD24^?/low BCSC phenotype and additionally show high expression of the BCSC markers CD49f and Sox2. Thus our results indicate that eHSP90 represents a potential novel BCSC marker. Moreover, we present evidence that eHSP90 is functionally involved in BCSC activity in vitro and in vivo. Selective neutralization of eHSP90, using the monoclonal antibody mAb 4C5, has the capacity to inhibit stem cell activity in vitro because the formation of mammosphere-derived colonies is dramatically reduced in its presence. In vivo, the treatment of mice with mAb4C5 using a prophylactic protocol, significantly inhibited the primary growth of MDA-MB-231 and mammosphere-derived tumors. More importantly, administration of this antibody in a therapeutic protocol caused a statistically significant regression of established tumors derived from MDA-MB-231 originating mammospheres. Tumor regression was even greater when mAb 4C5 was administered in combination with paclitaxel. Overall, our findings implicate eHSP90 as a potential novel BCSC biomarker. Moreover they show that eHSP90 participates in BCSC-derived primary tumor growth. Finally, we provide additional support for the possible therapeutic value of mAb4C5 in the treatment of breast cancer.     

The pyrrolo-1,5-benzoxazepine, PBOX-6, inhibits the growth of breast cancer cells in vitro independent of estrogen receptor status and inhibits breast tumour growth in vivo

Members of a novel series of pyrrolo-1,5-benzoxazepine (PBOX) compounds have been shown to induce apoptosis in a number of human leukemia cell lines of different haematological lineage, suggesting their potential as anti-cancer agents. In this study, we sought to determine if PBOX-6, a well characterised member of the PBOX series of compounds, is also an effective inhibitor of breast cancer growth. Two estrogen receptor (ER)-positive (MCF-7 and T-47-D) and two ER-negative (MDA-MB-231 and SK-BR-3) cell lines were examined. The 3,4,5-dimethylthiazol-2-yl-2,5-diphenyl-tetrazolium bromide (MTT) assay was used to determine reduction in cell viability. PBOX-6 reduced the cell viability of all four cell lines tested, regardless of ER status, with IC(50) values ranging from 1.0 to 2.3 microM. PBOX-6 was most effective in the SK-BR-3 cells, which express high endogenous levels of the HER-2 oncogene. Overexpression of the HER-2 oncogene has been associated with aggressive disease and resistance to chemotherapy. The mechanism of PBOX-6-induced cell death was due to apoptosis, as indicated by the increased proportion of cells in the pre-G1 peak and poly(ADP-ribose) polymerase (PARP) cleavage. Moreover, intratumoural administration of PBOX-6 (7.5 mg/kg) significantly inhibited tumour growth in vivo in a mouse mammary carcinoma model (p=0.04, n=5, Student's t-test). Thus, PBOX-6 could be a promising anti-cancer agent for both hormone-dependent and -independent breast cancers.     

PC-SPES inhibits colon cancer growth in vitro and in vivo

PC-SPES is a mixture of eight herbs with antiproliferative activity in prostate cancer cell lines and antitumor effects in animal models of prostate cancer. In addition, evidence of clinical efficacy in advanced prostate cancer has been reported. PC-SPES has also been shown to have antitumor activity against several other cancer cell lines including breast and neuroepithelial cancer, melanoma, and leukemia cell lines. Because of these findings, we investigated the effects of PC-SPES in vitro in colon cancer cell lines SW480, SW620, and DLD-1 and in vivo in the Apc(min) mouse, a murine model for intestinal carcinogenesis. For the in vitro studies, colon cancer cell lines were exposed to an ethanolic extract of PC-SPES compared with a diluent control [ethanol < or = 0.3% (v/v)]. PC-SPES resulted in a marked suppression of cell proliferation in all colon cancer cells studied. PC-SPES (3 micro l/ml) caused a 95% inhibition of cell proliferation of the DLD-1 colon cancer cell line, and similar results were observed in the SW480 and SW620 colon cancer cell lines. Cell cycle analysis demonstrated a drastic (> or =60%) accumulation of cells in the G(2)-M phase with a concomitant decrease of cells in the G(0)-G(1) phase in all colon cancer cell lines studied after treatment with PC-SPES (1.5 micro l/ml for 48 h). Western blot analysis demonstrated a decrease in protein levels of beta-tubulin in the SW620 cell line exposed to PC-SPES. Terminal deoxynucleotidyl transferase-mediated nick end labeling analysis revealed an increase in apoptotic colon cancer cells incubated with PC-SPES. For the in vivo studies, female 4-5-week-old Apc(min) mice were randomized to two groups: a PC-SPES-treated group (n = 11) received 250 mg/kg/day (0.2 ml) PC-SPES via gastrointestinal gavage; and a control group (n = 10) received 0.2 ml of the vehicle solution (1.5% carboxymethylcellulose with 0.2% Tween 20) via gastrointestinal gavage. Both groups were treated five times a week for 10 weeks. After treatment, the gastrointestinal tract was dissected for polyp scoring by two observers blinded to treatment. The Apc(min) mice given PC-SPES had a 58% reduction in tumor number and a 56% decrease in tumor load. No effect on either food intake or body weight was observed in the treated versus sham groups. The present study is the first to report the potent activity of PC-SPES against colon cancer. Both cell cycle arrest and apoptosis occurred after treatment with PC-SPES. This suggests that the components of this herbal mixture, either independently or in combination, acted in colon cancer, resulting in a drastic effect on tumor initiation and tumor progression.     

A novel human Fab antibody for Trop2 inhibits breast cancer growth in vitro and in vivo

Human trophoblastic cell surface antigen 2 (Trop2) has been suggested as an oncogene, which is associated with the different types of tumors. In this study, a human Fab antibody against Trop2 extracellular domain was isolated from phage library by phage display technology, and characterized by ELISA, FACS, fluorescence staining and Western blotting analysis. MTT, apoptosis assay and wound healing assay were employed to evaluate the inhibitory effects of Trop2 Fab on breast cancer cell growth in vitro, while tumor‐xenograft model was employed to evaluate the inhibitory effects on breast cancer growth in vivo. The results showed that Trop2 Fab inhibited the proliferation, induced the apoptosis and suspended the migration of MDA‐MB‐231 cells in a dose dependent manner. The expression caspase‐3 was activated, and the expression of Bcl‐2 was reduced while that of Bax was elevated in MDA‐MB‐231 cells by treating with Trop2 Fab. In addition, Trop2 Fab inhibited the growth of breast cancer xenografts and the expression of Bcl‐2 was reduced while that of Bax was elevated in xenografts. Trop2 Fab, which was isolated successfully in this research, is a promising therapeutic agent for the treatment of Trop2 expressing breast cancer.     

Reversal of the glycolytic phenotype by dichloroacetate inhibits metastatic breast cancer cell growth in vitro and in vivo

The glycolytic phenotype is a widespread phenomenon in solid cancer forms, including breast cancer. Dichloroacetate (DCA) has recently been proposed as a novel and relatively non-toxic anti-cancer agent that can reverse the glycolytic phenotype in cancer cells through the inhibition of pyruvate dehydrogenase kinase. We have examined the effect of DCA against breast cancer cells, including in a highly metastatic in vivo model. The growth of several breast cancer cell lines was found to be inhibited by DCA in vitro. Further examination of 13762 MAT rat mammary adenocarcinoma cells found that reversal of the glycolytic phenotype by DCA correlated with the inhibition of proliferation without any increase in cell death. This was despite a small but significant increase in caspase 3/7 activity, which may sensitize cancer cells to other apoptotic triggers. In vivo, DCA caused a 58% reduction in the number of lung metastases observed macroscopically after injection of 13762 MAT cells into the tail vein of rats (P = 0.0001, n ≥ 9 per group). These results demonstrate that DCA has anti-proliferative properties in addition to pro-apoptotic properties, and can be effective against highly metastatic disease in vivo, highlighting its potential for clinical use.     

Knockdown of c-Myc expression by RNAi inhibits MCF-7 breast tumor cells growth in vitro and in vivo

IntroductionBreast cancer is the leading cause of cancer death in women worldwide. Elevated expression of c-Myc is a frequent genetic abnormality seen in this malignancy. For a better understanding of its role in maintaining the malignant phenotype, we used RNA interference (RNAi) directed against c-Myc in our study. RNAi provides a new, reliable method to investigate gene function and has the potential for gene therapy. The aim of the study was to examine the anti-tumor effects elicited by a decrease in the protein level of c-Myc by RNAi and its possible mechanism of effects in MCF-7 cells.MethodA plasmid-based polymerase III promoter system was used to deliver and express short interfering RNA (siRNA) targeting c-myc to reduce its expression in MCF-7 cells. Western blot analysis was used to measure the protein level of c-Myc. We assessed the effects of c-Myc silencing on tumor growth by a growth curve, by soft agar assay and by nude mice experiments in vivo. Standard fluorescence-activated cell sorter analysis and TdT-mediated dUTP nick end labelling assay were used to determine apoptosis of the cells.ResultsOur data showed that plasmids expressing siRNA against c-myc markedly and durably reduced its expression in MCF-7 cells by up to 80%, decreased the growth rate of MCF-7 cells, inhibited colony formation in soft agar and significantly reduced tumor growth in nude mice. We also found that depletion of c-Myc in this manner promoted apoptosis of MCF-7 cells upon serum withdrawal.Conclusionc-Myc has a pivotal function in the development of breast cancer. Our data show that decreasing the c-Myc protein level in MCF-7 cells by RNAi could significantly inhibit tumor growth both in vitro and in vivo, and imply the therapeutic potential of RNAi on the treatment of breast cancer by targeting overexpression oncogenes such as c-myc, and c-myc might be a potential therapeutic target for human breast cancer.