QCM Detection of Adhesion, Spreading and Proliferation of Human Breast Cancer Cells (MCF-7) on a Gold Surface

The quartz crystal microbalance （QCM） was used to monitor the one-day incubation of human breast cancer cells （MCF-7） on the gold electrode. In combination with an optical microscope simulation experiment, the cell-population pictures at various stages, the QCM responses to the cells＇ adhesion, spreading and proliferation on the electrode surface were discussed. The △f0 and △R1 responses were found mainly from mixed effects of viscodensity and surface stress, and in proportion to the cell coverage, rather than to the number of cells at the electrode. The significant fore-and-aft changes in cyclic voltammetry and electrochemical impedance spectroscopy of the ferri-ferrocyanide redox couple also proved that the cells were adhesion to the gold surface.

Dietary Daidzein Enhances Antiapoptotic Effect of 17β-Estradiol (E_2) on Breast Cancer MCF-7 Cells

Objective： To investigate whether dietary daidzein interact with endogenous 17β-Estradiol （E2） to give rise to additive or inhibitory effects on proliferation and apoptosis in breast cancer cells. Methods： Cell cycle distribution and apoptosis induction were analyzed by using flow cytometry when breast cancer cell lines MCF-7 were cotreated with daidzein （1, 5 μmol/L） and E2 （0.1-10 nmol/L） for 5 days. Whether daidzein could alter E2-modulated mRNA expression of estrogen receptor alpha （ERα）, estrogen receptor beta （ERI3） and ERβ-estrogen response element （ERE） dependent transcription was investigated by RT-PCR and luciferase induction assays. The effects of daidzein on E2-modulated expression of proapoptotic p53, bax and antiapoptotic bcl-2 at both mRNA and protein levels were also investigated by RT-PCR and Western blot. Results： Daidzein enhanced the antiapoptotic effect in an Ea dose-dependent manner, but had no effect on E2-induced proliferation. Daidzein antagonized E2-induced ERβ mRNA expression and ERβ-ERE dependent transcription. In addition, daidzein only antagonized E2-upregulated expression of p53 and bax, but had no effect on E2-upregulated expression of bcl-2. Conclusion： Daidzein enhances the antiapoptotic effect of E2 on breast cancer cells by inhibiting E2-mediated p53-bax proapoptotic pathway. These results suggest that dietary daidzein may enhance deleterious effect of endogenous E2 in hormone-dependent breast cancer.

EFFECT OF CIS-9, TRANS-11-CONJUGATED LINOLEIC ACID ON CELL CYCLE OF MAMMARY ADENOCARCINOMA CELLS(MCF-7)

Objective: To determine the effect of cis-9, trans-1 1-conjugated linoleic acid on the cell cycle of mammary cancer cells (MCF-7) and the possible mechanism of the inhibitory effect of c9,t11-CLA. Methods: Using cell culture and immunocytochemical techniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B1, D1, p16ink4a and p21cip/waf1 of MCF-7 cells at various c9,t11-CLA concentrations (25μM, 50μM, 100μM and 200μM), at 24h and 48h. 96% ethand was used as negative control. Results: The cell growth and DNA synthesis of MCF-7 cells were inhibited by c9,t11-CLA. After treatment with various doses of c9,t11-CLA mentioned above for 8 days, the inhibition frequency was 27.18%, 35.43%, 91.05%, and 92.86%, respectively. Inhibitory effect of c9,t11-CLA on DNA synthesis (except for 25μM, 24h) was demonstrated by significantly less incorporation of 3H-TdR than the negative control (P<0.05 and P<0.01). To further investigate the influence of the cell cycle progression, we found that c9,t11-CLA may arrest the cell cycle of MCF-7 cells. Immunocytochemical staining demonstrated that incubation with different concentration of c9,t11-CLA at various times significantly decreased the expression of PCNA, Cyclin A, B1, D1 in MCF-7 cells compared to the negative control (P<0.01), whereas the expression of p16ink4a and p21cip/waf1, cyclin-dependent kinases inhibitors (CDKI), were increased. Conclusions: The cell growth and proliferation of MCF-7 cells is inhibited by c9,t11-CLA via blocking cell cycle, accompanying reduced expression of cyclin A, B1, D1 and enhanced expression of CDKI (p16ink4a and p21cip/waf1).

Studies on mechanism of cis9,trans11-CLA and trans10,cis12-CLA inducing apoptosis of human breast cancer cell line MCF-7

Objective： The aim of the study was to explore the activities of cis9, trans11-CLA （C9, t11-CLA） and transl0, cis12-CLA （t10, c12-CLA） inhibiting tumor, and investigate their relationships with PPARy and apoptotic proteins, and mechanism of anti-cancer. Methods： The inhibitory rate, cell growth curve and apoptotic morphological observation of MCF-7 cells were obtained by MTT assay, trypan blue staining and Hoechst33342 fluorescence staining. The apoptotic rate and cell cycle were detected with flow cytometry. Transcriptional level of genes was detected with RT-PCR semi-quantitative method, and Western blot was performed to detect proteins levels. Results： The two CLA isomers could reduce cell proliferation （P 〈 0.05）, increase apoptotic rate （P 〈 0.05）, and increase obviously the transcriptional and protein levels of PPARy （P 〈 0.01）. The synchronism and correlation between the effects of CLA to PPARy and apoptotic proteins Bax, Bcl-2, Caspase 3 changes were found with the dose- and time-dependent manners. There was cooperative relation between the levels of PPARy and the rates of Bax/Bcl-2, Caspase 3 （small fragment） by experiments of PPARy inhibitor GW9662 and ligand Rosiglitazone. Conclusion： The apoptotic pathway of PPARy-Bcl-2-Caspase 3 signaling was found. The C9, t11-CLA and tl0, c12-CLA could inhibit MCF-7 cell proliferation and promote apoptosis via activating PPARy-Bcl-2-Caspase 3 pathway. CLA may be a kind of activator of PPARv.

Cytotoxic Activity of <i>Thelesperma megapotamicum</i>Organic Fractions against MCF-7 Human Breast Cancer Cell Line

Thelesperma megapotamicum (Asteraceae) is commonly used in Argentine to treat various diseases (renal, digestive affections, and as anaesthesia). The present study showed the mechanisms involved “in vitro” cytotoxicity of T. megapotamicum Fractions. Five Fractions (F1 - F5) were separated by column chromatography (Silica gel) using hexane:diethyl ether as eluents. Viability was evaluated in Human breast carcinoma cell line (MCF-7) by staining with crystal violet. With respect to F1 Fraction treatment, the cell survival was 49.14% ± 8.87%, while the F2 and F3 ones exhibited a strong reduction of cell viability to only 26.35% ± 1.63% and 23.3%1 ± 0.53% of the control cell at 50 μg/ml, respectively. Apoptotic effect of these Fractions was detected using FITC-labeled Annexin V and propidium iodide binding assays and was confirmed by a higher proportion of apoptotic cells due to F2 and F3 treatments. T. megapotamicum active Fractions could facilitate the tumoral cells death by decreasing the activity of the enzyme Gamma-glutamyltranspeptidase and causing alteration in cell membrane sialoglycoconjugates and others involved anticancer mechanisms including apoptosis.

Study on Cisplatin Aggravating DNA Damage and Causing a High Apoptosis Rate on Breast Cancer MCF-7 Cells

[Objectives] To investigate the mechanism of DNA damage of cisplatin( DDP),a broad spectrum anticancer drug on breast cancer MCF-7 cells,and to study the mechanism of apoptosis induced by DDP.[Methods]MCF-7 cells were treated by DDP( 0 mg/L,2 mg/L,4 mg/L,6 mg/L,6 mg/L,and 10 mg/L) for 48 hours. MTT assay was used to detect the inhibitory effect of DDP on MCF-7 cells and IC50 value was calculated. Western blot was adopted to detect the expression of γ-H2 AX,which was the marker of DNA double stranded breaks( DSBs) and ATM( sensory molecules of DSBs),the apoptotic signal transduction molecule cleaved caspase-3,and the proteins associated with apoptosis calpain.[Results]DDP inhibited MCF-7 cell activity in a concentration-dependent manner and IC50 was 7. 57 mg/L. In contrast to the control group( without DDP treatment),MCF-7 cells with DDP treatment expressed more γ-H2 AX,ATM,cleaved caspase-3 and calpain.[Conclusions] DDP could inhibit the activity of breast cancer MCF-7 cells. Its mechanisms may be associated with inhibition of MCF-7 cell apoptosis,induction of DNA double strand breaking and the expression of pro-apoptotic protein up-regulation.

Inhibition of cell proliferation by siRNA targeting hPRLR in breast cancer MCF-7 cell line

Objective： To study the inhibition of proliferation of breast cancer by small interfering RNA（siRNA） targeting human prolactin （hPRLR） and the underlying mechanisms. Methods：The siRNA targeting hPRLR was chemically synthesized and transfected into MCF-7 cells, the expression of hPRLR was analyzed by real-time quantitive PCR, cell growth inhibition was measured with MTT assay, cell cycle of the transfected cells was examined by flow cytometry, meanwhile, expression of cyclin D1 was tested by semi-quantitative RT-PCR, Results：24 h after transfection with 100 nmol/L siRNA-PRLR, the expression of hPRLR mRNA was suppressed by 65%, cells in G1 phase increased, but cells in S phase decreased. Down regulated hPRLR expression exhibited significant inhibition in cell proliferation. And the expression of cyclin D 1 was down regulated. Conclusion：The results indicate that siRNA-hPRLR is a useful tool for silencing hPRLR expression and inhibiting cell proliferation in breast cancer MCF-7 cell line, and it may be a possible new approach for breast cancer gene therapy.

Piperine suppresses growth and migration of human breast cancer cells through attenuation of Rac1 expression

Objective:To investigate the effect of piperine on human breast cancer cells.Methods:The effect of piperine on proliferation and migration of human breast cancer cells,MCF-7 and MDA-MB-231,was investigated using colony formation assays,wound healing assays,Matrigel migration assays,flow cytometry,RT-qPCR,and Western blotting assays.Results:Piperine inhibited the growth of MCF-7 and MDA-MB-231 cells and suppressed colony formation.Cell reduction at the G_(0)/G_(1) phase and cell arrest at the G_(2)/M phase were observed in breast cancer cells.However,the significant effect was only demonstrated in MDA-MB-231 cells.Moreover,cancer cell migration was suppressed by piperine at low concentration.RT-qPCR and Western blotting assays showed that piperine downregulated Rac1 gene and protein expression.Conclusions:Piperine could inhibit growth and migration of breast cancer cells by reducing Rac1 gene and protein expression.

Breast Cancer MCF-7 Cell Spheroid Culture for Drug Discovery and Development

In vitro 3D cancer spheroids (tumoroids) exhibit a drug resistance profile similar to that found in solid tumors. 3D spheroid culture methods recreate more physiologically relevant microenvironments for cells. Therefore, these models are more appropriate for cancer drug screening. We have recently developed a protocol for MCF-7 cell spheroid culture, and used this method to test the effects of different types of drugs on this estrogen-dependent breast cancer cell spheroid. Our results demonstrated that MCF-7 cells can grow spheroid in medium using a low attachment plate. We managed to grow one spheroid in each well, and the spheroid can grow over a month, the size of the spheroid can grow over a hundred times in volume. Our targeted drug experimental results suggest that estrogen sulfotransferase, steroid sulfatase, and G protein-coupled estrogen receptor may play critical roles in MCF-7 cell spheroid growth, while estrogen receptors α and β may not play an essential role in MCF-7 spheroid growth. Organoids are the miniatures of in vivo tissues and reiterate the in vivo microenvironment of a specific organ, best fit for the in vitro studies of diseases and drug development. Tumoroid, developed from cancer cell lines or patients’ tumor tissue, is the best in vitro model of in vivo tumors. 3D spheroid technology will be the best future method for drug development of cancers and other diseases. Our reported method can be developed clinically to develop personalized drugs when the patient’s tumor tissues are used to develop a spheroid culture for drug screening.

Effect of Guizhi Fuling capsule and its extracts on human breast cancer cells proliferation

OBJECTIVE To evaluate the effect of Guizhi Fuling Capsule active pharmaceutical ingredient(API)and its fractions on human breast cancer cells proliferation by high-throughput screening assay.METHODS The crude fractions were obtained from the extraction and elution of the API of Guizhi Fuling Capsule,and 929 standard fractions were obtained by the optimal separation conditions.Sulforhodamine B(SRB)method was used to evaluate the effects of the Guizhi Fuling capsule API and929 kinds of fractions on the proliferation of human breast cancer cells MCF-7 and MDA-MB-231.RESULTS The Guizhi Fuling capsule API had a strong ability to inhibit the proliferation of MCF-7 cells at high concentration and the ability to inhibit MDA-MB-231 cells' proliferate at low concentration following 72 h treatment;some samples of 929 fractions(5μg·mL^(-1))was found to have a breast cancer cell growth inhibition rate above 50%,without toxicity on HUVECs proliferation.CONCLUSION The API of Guizhi Fuling capsule had significant cytotoxicity effects on these two human breast cancer cells,with significant concentration-and time-dependent manner.

REVERSION OF MULTIDRUG RESISTANCE IN THE P-GLYCOPROTEIN POSITIVE BREAST CANCER CELL LINE(MCF-7/ADR) BY INTRODUCTION OF HAMMERHEAD RIBOZYME

A hammerhead ribozyme which site-specifically cleaved the GUC position in canon 880 of the mdr1 mRNA was designed. The target site was chosen between the two ATP binding sites, which may be important for the function of the P-Gp as an ATP-dependent pump. A DNA sequence encoding the ribozyme gene was then incorporated into a eukaryotic expression vector (pH Apr-1 neo) and transfected into the breast cancer cell line MCF-7/Adr, which is resistant to adriamycin and expresses the MDR phenotype. The ribozyme was stably expressed in the cell line by the RNA dot blotting assay. The result of Northern blot assay showed that the expressed ribozyme could decrease the level of mdrl mRNA expression by 83. 5 %; and the expressed ribozyme could inhibite the formation of p-glycoprotein detected by immuno- cy-tochemistry assay and could reduce the cell’s resistance to adrimycin; this means that the resistant cells were 1 000-fold more resistant than the parental cell line(MCF-7), whereas those cell clones that showed ribozyme expression were only 6-fold more resistant than the parental cell line. These results show that a potentially useful tool is at hand which may inactivate MDR1 mRNA and revert the multidrug resistance phenotype.

Synthesis and Characterization of Trithiocarbonate-Organoclays Nanohybrids and Their Interaction with MCF-7 Cancer Cells

This work presents a new approach for the fabrication of organic/inorganic nanohybrids as anticancer drugs by an intercalation method using S,S-bis（α,α′-dimethyl-α″-acetic acid） （trithiocarbonate） as a modifier and two organoclays, such as reactive octadecylamine/MMT （montmorillonite） and non-reactive dimethyldidodecyl ammonium/MMT. The chemical and physical structures and the surface morphology of these covalently and non-covalently linked nanohybrids were investigated by FT-IR （Fourier translbrm infrared） spectroscopy, ^13C and ^29Si solid state NMR （nuclear magnetic resonance） spectroscopy, XRD （X-ray powder diffraction） and SEM （scanning electron microscopy） analyses, respectively. To evaluate the anticancer activities of the novel BATC/organoclay hybrids against MCF-7 breast cancer cells, a combination of different biochemical and biophysical testing techniques were used. Cell proliferation and cytotoxicity were detected in vitro using a real-time analysis. Cell death was confirmed by using apoptotic and necrotic analyses, the effects of which were detennined by the double staining and Annexin-V-FLUOS testing method. The results demonstrate that intercalated hybrid complexes containing a combination of various anticancer sites, such as free and complexed carboxyl, trithiocarbonate, amine and ammonium cations significantly induced cell death in breast cancer via their interactions with the DNA macromolecules of cancer cells by destroying the self-assemb｜ed structure of growing cells. Fabricated hybrid complexes may represent a new generation of effective and selective anticancer drug systems with a synthetic/natural origin for cancer chemotherapy.

毛酸浆内酯通过抑制STAT3诱导人乳腺癌MCF-7细胞凋亡

[目的]旨在探讨信号转导和转录激活因子3(STAT3)在毛酸浆内酯(PPB)诱导人乳腺癌MCF-7细胞凋亡中发挥的作用。[方法]采用荧光染色法分析PPB诱导MCF-7细胞凋亡;使用生物信息学方法预测PPB抗乳腺癌的潜在机制;采用噻唑蓝(MTT)法考察STAT3抑制剂S3I-201以及STAT3小干扰RNA(siRNA)对PPB抑制MCF-7细胞生长的作用;采用蛋白免疫印迹(Western Blot)法考察PPB单独处理或STAT3 siRNA预处理后对MCF-7细胞中STAT3、B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、半胱氨酸天冬氨酸蛋白酶8(Caspase8)、半胱氨酸天冬氨酸蛋白酶9(Caspase9)、细胞色素c(Cytochrome c)以及多聚ADP核糖聚合酶(PARP)蛋白表达的影响。[结果]MCF-7细胞经PPB作用后凋亡形态特征明显,凋亡比例上升;生物信息学结果显示PPB与乳腺癌疾病的共同靶点STAT3在乳腺癌组织中高表达,单基因GSEA结果提示STAT3高表达与凋亡信号通路呈负相关;Western Blot法检测结果显示PPB能够抑制STAT3的磷酸化;S3I-201抑制剂或siRNA敲降STAT3均能进一步促进PPB抑制MCF-7细胞生长;此外,敲降STAT3进一步增加PPB对促凋亡蛋白Bax、Cytochrome c、裂解的Caspase8(Cleaved-Caspase8)、裂解的Caspase9(Cleaved-Caspase9)以及裂解的PARP(Cleaved-PARP)的促进作用,并增加PPB对抗凋亡蛋白Bcl-2的抑制作用。[结论]PPB通过抑制STAT3诱导人乳腺癌MCF-7细胞凋亡。

Cytotoxicity screening of Melastoma malabathricum extracts on human breast cancer cell lines in vitro

Objective:To screen the cytotoxic activity of Melasloma malabathricum(M,malubathricum)against human breast carreer cell line(MCF-7)in vitro.Methods:A three steps extraction protocol using n-hexane,chloroform and methanol as the solvents systems was carried out on leaves,stems and flowers of M.nalabathricum.Dimethyl sulfoxide was used in extracts dilution and serial dilutions were conducted to obtain five different extract concentrations(100μg/mL,50μg/mL,25μg/mL,123μg/rnL and 6.25μg/mL).The evaluation of cell growth was determined using methylene blue assay.Results:Methanol extract from the leaves showed significant anticancer activity against MCF-7cell lines with the TC_(50)value of 7.14μg/ml while methanol and chloroform extract from the flowers exhibited a moderate activity towards MCF-7 cell line,with the IC_(50)value of 33.63μg/mL and 45.76μg/mL respectively after 72 h of treatment.Conclusions:The extracts from leaves and flowers of M.nulabatkricum showed promising anticancer activity toward human breast cancer cell lines with the lowest IC_(50)at 7.14μg/mL while the extracts from stems showed less growth inhibition activity.

Sensitivity Evaluation of Two Human Breast Cancer Cell Lines to Tamoxifen through Apoptosis Induction

Tamoxifen citrate (TAM) has been used to treat breast cancer in women for many years. The com-parative effects of TAM in inducing apoptosis were evaluated in estrogen receptor-positive (ER- positive MCF-7) and estrogen receptor-negative (ER-negative MDA-MB-231) human breast cancer cell lines in vitro in order to determine if these two cell lines differ in their sensitivity to TAM. Mi-tochondrial membrane permeability potential disruption was assessed in both cell lines by a lip-ophilic cationic dye (DePsipher assay, Trevigen, Inc.) utilizing fluorescence microscopy. Using this specific fluorochrome, we were able to associate mitochondrial membrane disruption to early, mid-, and late apoptotic cells. TAM induced cell death via apoptosis in both ER-positive and ER- negative cells, however, apoptosis induction was more pronounced in ER-positive MCF-7 compared to ER-negative MDA-MB-231 breast cancer cells. These findings may have some therapeutic use in the treatment of estrogen dependent and estrogen independent breast cancer.

粉防己碱逆转人乳腺癌MCF-7多药耐药细胞的抗凋亡作用

目的 :研究粉防己碱与长春新碱合用能否逆转人乳腺癌MCF 7多药耐药细胞的抗凋亡作用。方法 :用荧光染料Hoechst 3334 2和碘化丙锭联染观察染色质凝集 ,流式细胞术检测G1亚峰 ,TUNEL法检测凋亡细胞 ,Fluo 3染色法测定细胞内游离钙。结果 :抗肿瘤药物长春新碱处理MCF 7敏感和耐药细胞后 2 4h ,可观察到 2种类型的染色质凝集 ;但在耐药细胞中 ,相同浓度处理下染色质凝集的细胞明显减少。无明显细胞毒性的粉防己碱(2 0 μmol·L-1)与长春新碱合用 ,荧光显示法和TUNEL法均证实敏感和耐药的凋亡细胞明显增多。粉防己碱与长春新碱合用明显升高细胞内的游离钙含量。结论 :粉防己碱能有效地逆转人乳腺癌MCF

苦丁茶对MCF-7人乳腺癌细胞的体外抗癌效果

对市售的苦丁茶进行MCF-7人乳腺癌细胞体外抗癌效果和体内抗转移效果评价.通过MTT实验、DAPI荧光染色分析和RT-PCR分析说明其体外抗癌效果.200μg/mL苦丁茶(81%抑制率)水提物表现出对MCF-7人乳腺癌细胞较强的生长抑制效果.200μg/mL比100和50μg/mL苦丁茶水提物具有更强的细胞诱导凋亡效果,Bax,caspase-3和caspase-9的mRNA表达得到增强,Bcl-2表达减弱.苦丁茶水提物处理后炎症相关因子NF-κB,iNOS和COX-2表达减弱,展示了苦丁茶的抗炎特性.由此得出,一定质量浓度的苦丁茶具有良好的抗癌预防效果.

紫龙金对人乳腺癌细胞系MCF-7增殖及凋亡的影响

目的观察复方中药紫龙金对人乳腺癌细胞系MCF-7增殖的抑制作用及对其凋亡的诱导作用,探讨紫龙金治疗乳腺癌的作用机制。方法依据培养液紫龙金浓度的差异,实验共设4组:(1)对照组:不加紫龙金干预的1640培养液;(2)紫龙金低浓度组:1.5 mg生药/mL紫龙金培养液;(3)紫龙金中浓度组:3 mg生药/mL紫龙金培养液;(4)紫龙金高浓度组:6 mg生药/mL紫龙金培养液。采用细胞计数法绘制生长曲线及四甲基偶氮唑蓝(MTT)比色法检测不同浓度紫龙金对MCF-7细胞增殖能力的影响,并应用流式细胞术、Hoechst 33342核染色法及DNA梯度形成法测定紫龙金诱导凋亡的作用。结果(1)与对照组比较,紫龙金各剂量组的细胞计数在各时间点(24、48、72、96、120、144 h)明显减少,其差异均有统计学意义(P<0.05);紫龙金各剂量组间的生长抑制率差异除低、中浓度组间在24、72 h无统计学意义外(P>0.05),各剂量组间两两比较在不同时间点(24、48、72、96、120、144 h),其差异均有统计学意义(P<0.05)。紫龙金对MCF-7细胞的增殖抑制作用呈时间依赖性和剂量依赖性;(2)紫龙金使细胞阻滞在G_0/G_1期;(3)中、高浓度紫龙金诱导MCF-7细胞凋亡,并形成DNA ladder。结论紫龙金能抑制人乳腺癌细胞MCF-7细胞增殖,并诱导细胞凋亡,从而起到抗肿瘤的作用。

共轭亚油酸异构体对人乳腺癌MCF-7细胞增殖的抑制和促凋亡作用

共轭亚油酸（conjugated linoleic acid,CLA）是一组具18个碳原子,含有共轭双键的多不饱和脂肪酸,是必需脂肪酸亚油酸的同分异构体.近年来大量动物试验表明,CLA具有抗癌[1]、抗动脉粥样硬化[2]、降低脂肪沉积[3]等重要生理功能.虽然目前国内外关于CLA对癌细胞凋亡的影响已做了大量研究工作.

大蓟炭中香叶木素诱导人乳腺癌MCF-7细胞凋亡及其机制研究

研究大蓟炭中香叶木素诱导人乳腺癌MCF-7细胞凋亡及其作用机制。采用硅胶和Sephadex LH-20柱层析从大蓟炭中分离鉴定了三个黄酮类化合物,经NMR和MS鉴定他们的结构分别为香叶木素(1)、刺槐素(2)和柳川鱼黄素(3)。采用MTS方法检测不同浓度的香叶木素对MCF-7的细胞活力的影响;流式细胞术检测不同浓度的香叶木素处理对MCF-7细胞凋亡的作用;Western blot法检测香叶木素处理对细胞PARP、P-JNK等细胞凋亡相关蛋白表达的影响。MTS及流式细胞术结果显示香叶木素能显著抑制MCF-7的增殖并且诱导细胞凋亡;香叶木素可上调P-JNK促进细胞凋亡。结果表明香叶木素在体外实验能通过激活JNK细胞凋亡通路抑制MCF-7的增殖及促进细胞凋亡。