Methanolic extract of Abrus precatorius promotes breast cancer MDA-MB-231 cell death by inducing cell cycle arrest at G0/G1 and upregulating Bax

Objective:To determine the anti-proliferative activity of Abrus precatorius(A.precatorius)leaf extracts and their effect on cell death.Methods:A.precatorius leaves were extracted successively with hexane,ethyl acetate and methanol by Soxhlet extraction.Aqueous extract was prepared by decoction at 50 ℃.Extracts of A.precatorius leaves were used to treat selected cancer and normal cell lines for72 h.Furthermore,3-(4,5-dimethyl thiazol-2-yl)2,5-diphenyl tetrazolium bromide assay was performed to determine cell viability.Analysis of cell cycle arrest,apoptosis assay and apoptosis protein expressions were determined by flow cytometry.Results:Methanolic extract of A.precatorius leaves showed the lowest IC50 on MDA-MB-231 cells at(26.40±5.40)μg/mL.Flow cytometry analysis revealed that cell arrest occurred at G0/G1 phase and the apoptosis assay showed the occurrence of early apoptosis at 48 h in MDAMB-231 cells treated with methanolic extract of A.precatorius leaves.Methanolic extract of A.precatorius leaves induced apoptosis by upregulation of Bax,p53 and caspase-3 and downregulation of Bcl-2.Conclusions:Methanolic extract of A precatorius leaves promotes MDA-MB-231 cell death by inducing cell cycle arrest and apoptosis possibly via the mitochondrial-related pathway.

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.

Meclizine Chloridrate and Methyl-β-Cyclodextrin Associated with Monophosphoester Synthetic Phosphoethanolamine Modulating Proliferative Potential in Triple-Negative Breast Cancer Cells

Synthetic phosphoethanolamine(Pho-s)is a monophosphoester ester with anti-inflammatory and pro-apoptotic properties.Meclizine chloridrate(MC)is a histamine H1 receptor blocker that is also able to inhibit cellular respiration.However,MC does not inhibit cellular respiration in isolated mitochondria such as antimycin and rotenone.Methyl-β-cyclodextrin(MβCD)belongs to theβ-cyclodextrin family,which is capable of removing cholesterol from the plasma membrane.The aim of this study was to evaluate the proliferative effects of meclizine chloridrate and methyl-β-cyclodextrin compounds associated with synthetic phosphoethanolamine in a triple-negative human breast tumor line,MDA-MB-231 Cell viability of the tumor line and normal cells FN1 was evaluated by MTT colorimetric test;the production of free radicals was determined by lipoperoxidation(LPO)test;and the percentage of cell cycle phases and proliferative index was evaluated by flow cytometry.Cell viability demonstrated a significant decrease with the treatments of MβCD,MC and Pho-s associated with MC.The production of free radicals decreases significantly in all treatments.In addition,a significant increase of DNA fragment and decrease in G0/G1 cell cycle phase were observed in cellular percentage with concentrations of 20 and 30 mM of Pho-s in association with MC and MβCD,respectively.

Effects of bisphenol compounds on the growth and epithelial mesenchymal transition of MCF-7 CV human breast cancer cells

Bisphenol-A（BPA） has been considered as an endocrine disrupting chemical（EDC） because it can exert estrogenic properties.For bisphenol-S（BPS） and bisphenol-F（BPF） that are BPA analogs and substitutes,their risk to estrogendependent cancer has been reported rarely compared with the numerous cases of BPA.In this study,we examined whether BPA,BPS,and BPF can lead to the proliferation,migration,and epithelial mesenchymal transition（EMT） of MCF-7 clonal variant（MCF-7 CV） breast cancer cells expressing estrogen receptors（ERs）.In a cell viability assay,BPA,BPS,and BPF significantly increased proliferation of MCF-7 CV cells compared to control（DMSO） as did17β-estradiol（E2）.In Western blotting assay,BPA,BPS,and BPF enhanced the protein expression of cell cycle progression genes such as cyclin D1 and E1.In addition,MCF-7 CV cells lost cell to cell contacts and acquired fibroblast-like morphology by the treatment of BPA,BPS,or BPF for 24 hours.In cell migration assay,BPA,BPS,and BPF accelerated the migration capability of MCF-7 CV cells as did E2.In relation with the EMT process,BPA,BPS,and BPF increased the protein expression of N-cadherin,while they decreased the protein expression of Ecadherin.When BPA,BPS,and BPF were co-treated with ICI 182,780,an ER antagonist,proliferation effects were reversed,the expression of cyclin D1 and cyclin E1 was downregulated,and the altered cell migration and expression of N-cadherin and E-cadherin by BPA,BPS,and BPF were restored to the control level.Thus,these results imply that BPS and BPF also have the risk of breast cancer progression as much as BPA in the induction of proliferation and migration of MCF-7 CV cells by regulating the protein expression of cell cycle-related genes and EMT markers via the ER-dependent pathway.

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.

Investigating the effects of Pentoxifylline on human breast cancer cells using Raman spectroscopy

Breast cancer is one of the leading causes of cancer-related deaths in a global scenario.In the present study,biochemical changes exerted upon Pentoxifylline(PTX)treatment had been ap-praised in human breast cancer cells using Raman spectrosecopy.There are no clinically approved methods to monitor such therapeutic responses available.The spectral profiling is suggestive of changes in DNA,protein and lipid contents showing a linear relationship with drug dosage.Further,multivariate analysis using principal component based linear-discriminant-analysis(PC-LDA)was employed for dlassifying the control and the PTX treated groups.These findings support the feasibility of Raman spectroscopy as an alternate/adjunct label-free,objective method for monitoring drug-induced modifications against breast cancer cells.

Anticancer property of sediment actinomycetes against MCF-7 and MDA-MB-231 cell lines

Objective:To investigate the anticancer property of marine sediment actinomvceles against two different breast cancer cell lines.Methods:In vitro anticancer activity was carried out against breast(MCF-7 and MDA-MB-231)cancer cell lines.Partial sequences of the 16s rRNA gene,phylogenetic tree construction,multiple sequence analysis and secondary structure analysis were also carried out with the actinomycetes isolates.Results:Of the selected five actinomycete isolates,ACT01 and ACT02 showed the IC_(50)value with(10.13±0.92)and(22.34±5.82)μg/mL concentrations,respectively for MCF-7 cell line at 48 h,but ACT01 showed the minimum(18.54±2.49μg/mL)level of IC_(50)value with MDA-MB-231 cell line.Further,the 16s rRNA partial sequences of ACT01,ACT02,ACT03,ACT04 and ACT05 isolates were also deposited in NCBI data bank with the accession numbers of GQ478246,GQ478247,GQ478248,GQ478249 and GQ478250.respectively.The phylogenetic tree analysis showed that,the isolates of ACT02 and ACT03 were represented in groupⅠandⅢ,respectively,but ACT01 and ACT02 were represented in groupⅡ.The multiple sequence alignment of the actinomycete isolates showed that,the maximum identical conserved regions were identified with the nucleotide regions of 125 to 221st base pairs,65 to 119th base pairs and 55,48 and 31st base pairs.Secondary structure prediction of the 16s rRNA showed that,the maximum free energy was consumed with ACT03 isolate(-45.4 kkal/mol)and the minimum free energy was consumed with ACT04 isolate(-57.6 kkal/mol).Conclusions:The actinomycete isolates of ACT01 and ACT02(GQ478246 and GQ478247)which are isolated from sediment sample can be further used as anticancer agents against breast cancer cell lines.

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.

组蛋白去乙酰化酶抑制剂SAHA抑制乳腺癌细胞MDA-MB-435增殖及促凋亡的作用机制

目的观察组蛋白去乙酰化酶抑制剂SAHA对人乳腺癌细胞系MDA-MB-435增殖、凋亡等的作用及其相关分子机制。方法不同浓度的SAHA作用于MDA-MB-435细胞后,采用MTT、流式细胞分析、Western blot、荧光定量PCR等方法检测细胞增殖、凋亡、周期阻滞情况及相关蛋白及mRNA表达。结果 MTT检测结果表明SAHA可呈剂量依赖性抑制细胞增殖,流式细胞分析发现SAHA可导致G2/M期周期阻滞、线粒体膜电位下降、活性氧(ROS)产生并发生早期凋亡。同时,SAHA可下调周期蛋白cyclin B、活化p38-MAPK及JNK,抑制p53的表达且可能不是通过PI3K通路、P38 MAPK通路、ERK1/2通路和NF-κB、JNK通路起作用。结论 SAHA能抑制MDA-MB-435细胞增殖,诱导其周期阻滞及早期凋亡,活化细胞内相关增殖分子,可作为乳腺癌潜在的候选药物。

三氧化二砷诱导雌激素受体阴性乳腺癌细胞株MDA-MB-435s凋亡和bcl-2、bax表达关系的研究

目的观察不同浓度三氧化二砷(As2O3)诱导人乳腺癌细胞系MDA-MB-435s凋亡的情况及对bcl-2和bax表达的影响,初步探讨了其诱导凋亡的途径。方法不同浓度As2O3体外作用于MDA-MB-435s细胞24h后,采用TUNEL染色法和DNA梯状电泳法检测细胞凋亡情况,应用免疫组化法检测细胞中bcl-2和bax蛋白表达情况。结果As2O3作用后,DNA琼脂糖凝胶电泳法呈现凋亡DNA梯状条带;As2O3作用组的凋亡指数明显高于阴性对照组(P<0.05);bcl-2表达下调,bax表达上调。结论As2O3能诱导MDA-MB-435s细胞凋亡,上调bcl-2蛋白表达、下调bax蛋白表达是其诱导凋亡的途径之一。

乳腺癌细胞MDA-MB-435s中侧群细胞的分选及其与非侧群细胞的生物学特点比较

目的分离乳腺癌细胞MDA-MB-435s中的侧群细胞(sidepopulation cells,SP),并比较侧群细胞和非侧群细胞(non-side population cells,NSP)的基本生物学特点.方法经Hoechst33342染色后,利用流式细胞技术分选乳腺癌细胞MDA-MB-435s中SP和NSP 2个细胞亚群,比较2群细胞的形态、增殖和周期等特点.结果分选得到的SP细胞约占5.2%,其增殖速度较NSP细胞快,且细胞形态较粗大.NSP细胞的G1期所占比例为73.63%,高于SP细胞的G1期所占比例为54.16%.结论 SP和NSP细胞的形态有差异,SP细胞的增殖速度快于NSP细胞,NSP细胞的周期阻滞在G1期,提示SP细胞可能在乳腺癌细胞的生长过程中具有重要的作用.

Microfluidic chip enables single-cell measurement for multidrug resistance in triple-negative breast cancer cells

Aims:Triple-negative breast cancer patients are commonly treated with combination chemotherapy.Nonetheless,outcomes remain substandard with relapses being of a frequent occurrence.Among the several mechanisms that result in treatment failure,multidrug resistance,which is mediated by ATP-binding cassette proteins,is the most common.Regardless of the substantial studies conducted on the heterogeneity of cancer types,only a few assays can distinguish the variability in multidrug resistance activity between individual cells.We aim to develop a single-cell assay to study this.Methods:This experiment utilized a microfluidic chip to measure the drug accumulation in single breast cancer cells in order to understand the inhibition of drug efflux properties.Results:Selection of single cells,loading of drugs,and fluorescence measurement for intracellular drug accumulation were all conducted on a microfluidic chip.As a result,measurements of the accumulation of chemotherapeutic drugs(e.g.,daunorubicin and paclitaxel)in single cells in the presence and absence of cyclosporine A were conducted.Parameters such as initial drug accumulation,signal saturation time,and fold-increase of drug with and without the presence cyclosporine A were also tested.Conclusion:The results display that drug accumulation in a single-cell greatly enhanced over its same-cell control because of inhibition by cyclosporine A.Furthermore,this experiment may provide a platform for future liquid biopsy studies to characterize the multidrug resistance activity at a single-cell level.

RNA结合蛋白NONO通过影响SKP2、E2F8表达调控乳腺癌细胞增殖的研究

目的探讨不含POU结构域的八聚体核苷酸结合蛋白(NONO)是否通过影响S期激酶相关蛋白2(SKP2)和E2F转录因子8(E2F8)表达从而调控乳腺癌细胞增殖。方法收集2019年6月至2020年6月于该院接受乳腺癌根治术治疗的43例乳腺癌患者的乳腺癌组织及癌旁组织石蜡块。采用免疫组织化学SP染色检测NONO、SKP2和E2F8在组织中的表达。将MCF-7细胞分为MCF-7组(无特殊处理)、sh-NC-MCF-7组(加入sh-NC序列正义链的慢病毒LV3液)和sh-NONO-MCF-7组(加入含sh-NONO序列正义链的慢病毒LV3液)。检测sh-NONO的沉默效率,筛选稳定株。分析沉默NONO对乳腺癌细胞增殖能力、细胞周期以及SKP2和E2F8表达的影响。结果乳腺癌组织中NONO、SKP2和E2F8阳性表达率显著高于癌旁组织(P<0.05);与MCF-7和sh-NC-MCF-7组比较,sh-NONO-MCF-7组NONO蛋白表达水平降低(P<0.05),提示成功构建NONO沉默MCF-7细胞株;与MCF-7和sh-NC-MCF-7组比较,sh-NONO-MCF-7组增殖能力降低(P<0.05);与MCF-7和sh-NC-MCF-7组比较,sh-NONO-MCF-7组G_(0)/G_(1)期细胞比例显著增加,S期和G_(2)/M期细胞比例显著降低(P<0.05);与MCF-7和sh-NC-MCF-7组比较,sh-NONO-MCF-7组SKP2和E2F8蛋白表达水平以及SKP2和E2F8 mRNA相对表达水平均显著降低(P<0.05)。结论沉默NONO表达可通过下调SKP2和E2F8表达,诱导细胞周期阻滞,从而抑制乳腺癌细胞增殖。

益气活血方对乳腺癌MDA-MB-435S细胞和MDA-MB-231细胞的影响

目的:观察益气活血方对乳腺癌MDA-MB-435S细胞和MDA-MB-231细胞的影响。方法:采用四甲基偶氮唑蓝法观察益气活血方对人乳腺癌MDA-MB-435S细胞和MDA-MB-231细胞增殖的影响;釆用四甲基偶氮唑蓝法等观察益气活血方对MDA-MB-435S细胞和MDA-MB-231细胞黏附能力的影响;采用Transwell小室模型观察益气活血方对MDA-MB-435S细胞和MDA-MB-231细胞侵袭能力的作用。结果:益气活血方对MDA-MB-435S和MDA-MB-231细胞的增殖具有抑制作用,呈现时间和质量浓度依赖性(P<0.05)。益气活血方对MDA-MB-435S和MDA-MB-231细胞体外黏附具有抑制作用,当质量浓度为80mg·L-1时,对MDA-MB-435S细胞体外黏附抑制作用呈现时间依赖性(P<0.05);益气活血方对MDA-MB-231细胞体外黏附的抑制作用呈现时间和质量浓度依赖性(P<0.05)。益气活血方对MDA-MB-435S和MDA-MB-231细胞侵袭能力具有抑制作用,呈质量浓度依赖性(P<0.05)。结论:益气活血方可以通过抑制影响乳腺癌MDA-MB-435S细胞和MDA-MB-231细胞的增殖、黏附和侵袭,达到抑制乳腺癌转移的作用。

The molecular interaction of ADAMTS-1 and fibulin-1 and its potential contribution to breast cancer biology

Aim: Fibulins and ADAMTSs are two families of extracellular matrix proteins implicated in key functional and pathological processes. The fact that the fibulin-1 and ADAMTS-1 proteins interact raises new questions about the roles of these extracellular matrix proteins in modulating tumor progression. Herein, we described the functional implications of the interaction between fibulin-1 and ADAMTS-1 on the behavior of breast cancer cell lines. Methods: Fibulin-1 and ADAMTS-1 were exogenously expressed in MCF-7 and MDA-MB-231 cell lines to assay the effect of their interaction in cellular properties. Results: ADAMTS-1 expression exacerbates tumor effects in terms of proliferation, invasion and mammosphere formation. In contrast, the simultaneous expression of ADAMTS-1 and fibulin-1 impairs these effects. The analysis of the expression of both proteins in human breast cancer tissue arrays provides new insights into the complex roles of fibulin-1 and ADAMTS-1 in this type of tumor. ;Conclusion: Our results suggests that the interaction between ADAMTS-1 and fibulin-1 induces a pronounced anti-tumoral effect.

红花多糖通过阻断PI3K/Akt/mTOR通路诱导人乳腺癌MDA-MB-435细胞凋亡的机制研究

目的研究红花多糖通过阻断PI3K/Akt/mTOR通路诱导人乳腺癌MDA-MB-435细胞凋亡的作用及其作用机制。方法将MDA-MB-435细胞分为对照组和红花多糖0.5、1.0 mg/mL组。MTT法及流式检测仪分别检测不同质量浓度红花多糖对MDA-MB-435细胞生长及凋亡的影响;RT-PCR及Western blotting法分别检测不同质量浓度红花多糖对MDA-MB-435细胞PI3K、Akt、mTOR mRNA和蛋白表达的影响。结果与对照组比较,红花多糖0.5 mg/mL组MDA-MB-435细胞抑制率为(21.52±2.43)%,红花多糖1.0 mg/mL组细胞抑制率为(27.73±3.75)%,显著高于红花多糖0.5 mg/m L组(P<0.05);与对照组比较,红花多糖能够显著提高MDA-MB-435细胞凋亡率(P<0.01),且呈剂量依赖性。RT-PCR及Western blotting实验结果显示,与对照组比较,红花多糖能够使MDA-MB-435细胞中PI3K、Akt、mTOR mRNA和蛋白表达显著降低(P<0.05、0.01)。结论红花多糖能有效抑制MDA-MB-435细胞的生长,促进其凋亡,作用可能是通过对PI3K/Akt/mTOR通路的阻断实现的。

葫芦素B体外对乳腺癌细胞的生长抑制作用研究

目的观察葫芦素B(Cucurbitacin B)对非磷酸化STAT3人乳腺癌细胞系MCF-7和磷酸化STAT3人乳腺癌细胞系MDA-MB-435S的增殖抑制和诱导凋亡作用,为临床应用提供依据。方法用不同浓度的葫芦素B分别处理MCF-7和MDA-MB-435S细胞,48 h后用MTT法检测细胞增殖;用荧光显微镜观察细胞凋亡。结果MTT结果显示,葫芦素B对MCF-7和MDA-MB-435S细胞的增殖抑制作用具有明显的剂量依赖性,统计学分析提示,各实验组与对照组之间差异有统计学意义(P<0.05);荧光显微镜显示典型的细胞凋亡。结论葫芦素B对人乳腺癌细胞的增殖具有抑制作用(与STAT3的活化状态无关),诱导乳腺癌细胞凋亡,从而发挥抗肿瘤效应。

半夏总生物碱对人乳腺癌细胞增殖的抑制作用

目的探讨半夏总生物碱(total alkaloids from pinellia ternate,TATP)对人乳腺癌细胞株MDA-MB-435S增殖的影响。方法采用四甲基偶氮唑盐(methyl thiazolil tetracolium,MTT)比色法以及集落形成率实验,检测不同浓度的TATP对MDA-MB-435S细胞株的生长抑制作用。应用单细胞凝胶电泳分析检测TATP导致MDA-MB-435S细胞的DNA损伤情况。结果人乳腺癌细胞MDA-MB-435S经TATP处理后,其体外增殖能力受到明显抑制且与药物剂量、作用时间呈正相关,经TATP作用24、48、72h后的半数抑制浓度分别为:98.37μg/ml、52.16μg/ml、33.63μg/ml。单细胞凝胶电泳(single cell gel electrophoresis,SCGE)中,TATP组细胞尾DNA含量、尾长及尾动量与对照组有统计学差异(P<0.01),且呈现浓度依赖性。结论在体外培养条件下,TATP能明显抑制MDA-MB-435S细胞增殖,其机制可能与DNA的损伤作用有关。

树突状细胞标志分子在人乳腺癌中的表达及与T细胞的关系

目的通过观察人乳腺癌组织中CDlc、S-100、HLA-DR阳性细胞数和表达强度的变化及其与T细胞的关系,了解乳腺癌局部微环境的免疫状态,探讨树突状细胞与乳腺癌发生、发展的关系,为乳腺癌的生物治疗提供实验依据。方法收集手术切除的人乳腺癌组织和癌旁相对正常乳腺组织,用免疫组织化学方法和图像分析技术对20例乳腺癌标本进行检测。结果乳腺癌组织中CDlc、S-100和HLA-DR的表达强度均较相对正常乳腺组织明显减弱(P<0.05);CD1c+DC、S-100+DC、HLA-DR+DC、CD4+T细胞和CD8+T细胞的数量均较相对正常乳腺组织明显减少(P<0.05),且乳腺癌组织中CDlc+DC细胞的数量比S-100+DC细胞的数量减少更明显,HLA-DR+DC与CD4+T细胞的数量呈明显相关关系(r=0.998);结论树突状细胞表面标志分子在人乳腺癌组织中的表达总量下降,树突状细胞在抗乳腺癌的免疫反应中可能起重要作用;这为临床开展乳腺癌的生物治疗提供了实验依据。

乳腺癌术前中医辨证与肿瘤增殖因子相关性研究

目的:探讨乳腺癌术前中医辨证与肿瘤增殖因子DNA倍体、S期细胞比例及Ki-67表达的相关性。方法:对160例乳腺癌患者术前中医辨证分型,术后手术标本进行DNA倍体、S期细胞比例、Ki-67检测,并做相关性分析。结果:乳腺癌患者术前辨证为正虚毒炽者DNA倍体异倍体、S期细胞比例为高度及Ki-67阳性出现率高于肝郁痰凝组和冲任失调组。经统计学处理,有显著差异(P<0.05)。结论:乳腺癌术前中医辨证与肿瘤增殖因子DNA倍体、S期细胞比例及Ki-67表达有相关性,随着患者中医辨证为肝郁痰凝证、冲任失调证、正虚毒炽证的不同,肿瘤的增殖能力依次增强,预后也更差。