In vitro anti-proliferative and antioxidant studies on Devil's Club Oplopanax horridus

Devil's Club, Oplopanax horridus (OH), is a widely used folk medicine in Alaska and British Columbia for treating a variety of ailments including arthritis, fever and diabetes. HPLC profiling shows that numerous compounds are present in the 70% ethanolic extract of OH dry root bark powder. OH extract inhibited K562, HL60, MCF7 and MDA-MB-468 cell growth with the 50% inhibition (IC(50)) estimated at 1/2700, 1/1700, 1/500 and 1/2500 dilutions, respectively. Non-cytotoxic concentrations (相似文献   

白皮杉醇对三阴性乳腺癌细胞系MDA-MB-468抗肿瘤作用及机制

目的:考察白皮杉醇(PIC)对三阴性乳腺癌细胞MDA-MB-468增殖、凋亡及细胞周期的作用,并对其作用机制进行探讨。方法:采用噻唑蓝(MTT)比色法考察PIC(0,2.5,5.0,10.0,20.0,40.0,80.0,160.0μmol·L-1)对三阴性乳腺癌MDA-MB-468细胞成活率的影响,并计算半抑制率(IC50);采用碘化丙啶(PI)染色观察PIC(5.0,10.0,20.0μmol·L^-1)对MDA-MB-468细胞周期的影响;采用细胞凋亡检测(Annexin V-FITC/PI)双染法观察PIC(5.0,10.0,20.0μmol·L^-1)对三阴性乳腺癌MDA-MB-468细胞的诱导凋亡作用;采用蛋白免疫印迹法(Western blot)观察不同浓度PIC(5.0,10.0,20.0μmol·L^-1)对MDA-MB-468细胞增殖、凋亡蛋白的影响,并用Western blot对分泌型糖蛋白Wnt/β-连环蛋白(Wnt/β-catenin)信号通路相关蛋白进行检测。结果:MTT比色法结果显示,与空白组比较,PIC(5.0,10.0,20.0,40.0,80.0,160.0μmol·L^-1)可呈浓度依赖性地抑制MDA-MB-468细胞的增殖(P<0.05,P<0.01),IC50为(39.4±4.6)μmol·L^-1;作用48 h,PIC(5.0,10.0,20.0μmol·L^-1)呈浓度依赖性地升高MDA-MB-468细胞处于细胞周期G0/G1期细胞(P<0.01);呈浓度依赖性地诱导MDA-MB-468细胞凋亡(P<0.01),其中,PIC(20.0μmol·L^-1)诱导细胞凋亡率为49.87%;PIC(10.0,20.0μmol·L^-1)可明显降低MDA-MB-468细胞中β-catenin及原癌基因(C-myc),黏附因子(CD44)蛋白的表达水平(P<0.05,P<0.01);PIC(5.0,10.0,20.0μmol·L^-1)可显著抑制蛋白激酶B(Akt)磷酸化,p38丝裂原活化蛋白激酶(p38 MAPK)蛋白的磷酸化,B淋巴细胞瘤-2(Bcl-2)的蛋白表达水平(P<0.01);增强半胱氨酸天冬氨酸蛋白酶-3(Caspase-3),Bcl-2相关X蛋白(Bax)和磷酸化β-catenin的蛋白表达(P<0.01)。结论:PIC可能通过抑制Wnt/β-catenin信号通路抑制MDA-MB-468细胞增殖,并将细胞周期阻滞在G0/G1期,从而诱导其凋亡。     

In vitro culture studies of Sutherlandia frutescens on human tumor cell lines

Sutherlandia frutescens is a South African herb used traditionally by the natives to treat cancer, and more recently to improve the overall health in HIV/AIDS patients. Gas chromatography/mass spectrometer profiling and liquid chromatographic/mass spectral investigation confirmed and quantified the presence of canavanine, GABA and arginine in the herbal preparation used in this study. In vitro study demonstrated a concentration dependent effect of Sutherlandia on several tumor cell lines, with 50% inhibition (IC50) of proliferation of MCF7, MDA-MB-468, Jurkat and HL60 cells at 1/250, 1/200, 1/150 and 1/200 dilutions, respectively. Sutherlandia treatment did not induce HL60 differentiation along the macrophage/monocyte or granulocyte lineage. It demonstrated antioxidant activity in reducing free radical cations with an estimated activity of 0.5 microl of Sutherlandia extract equivalent to that of 10 microM of Trolox. However, it did not significantly suppress lipopolysaccharide stimulated nitric oxide production by murine macrophage/monocyte RAW 264.7 cells, nor did it significantly inhibit IL-1beta and TNF-alpha mRNA expression in RAW 264.7 cells. In conclusion, Sutherlandia ethanolic extract showed a concentration dependent antiproliferative effect on several human tumor cell lines but did not show significant antioxidant effects. Further studies are needed to explore the activities of this multipurpose South African herbal preparation.     

Inhibition of Cancer Cell Proliferation and Antiradical Effects of Decoction,Hydroalcoholic Extract,and Principal Constituents of Hemidesmus indicus R. Br.

Indian Sarsaparilla (Hemidesmus indicus R. Br.) is widely used in Indian traditional medicine. In the present work, we explored the effects of decoction, traditional Ayurvedic preparation, and hydroalcoholic extract, a phytocomplex more traditionally studied and commercialized as food supplement in western medicine, from the roots as possible source of chemicals with new functional potential linked to their nutritional uses. The antiproliferative and antioxidant properties were assayed. To test antiproliferative affects, different cancer cell lines, growing both as monolayers (CaCo2, MCF‐7, A549, K562, MDA‐MB‐231, Jurkat, HepG2, and LoVo) and in suspension (K562 and Jurkat) were used. The decoction showed strong activity on HepG2 cells, while the hydroalcoholic extracts were active on HepG2, LoVo, MCF‐7, K562, and Jurkat cell lines. Weak inhibition of cancer cell proliferation was observed for the principal constituents of the preparations: 2‐hydroxy‐4‐methoxybenzaldehyde, 2‐hydroxy‐4‐methoxybenzoic acid, and 3‐hydroxy‐4‐methoxybenzaldehyde that were tested alone. The antiradical activity was tested with 2,2‐diphenyl‐1‐picrylhydrazyl and 2,2′‐azinobis(3‐ethylbenzothiazoline‐6‐sulfonic acid)diammonium salt tests and inhibition of nitric oxide production in lipopolysaccharide‐stimulated RAW 264.7 macrophages. Interesting result has also been obtained for hydroalcoholic extract regarding genoprotective potential (58.79% of inhibition at 37.5 µg/mL). Copyright © 2015 John Wiley & Sons, Ltd.     

Cytotoxic Impact of Costunolide Isolated from Costus speciosus on Breast Cancer via Differential Regulation of Cell Cycle—An In‐vitro and In‐silico Approach

Costunolide, a sesquiterpene lactone, is a biologically active molecule found in most of the medicinally valuable plants. The present study aims to evaluate the anticancer property of costunolide isolated from Costus speciosus against breast cancer cell lines (MCF‐7 and MDA‐MB‐231). Costunolide effectively reduced the viability of both MCF‐7 and MDA‐MB‐231 cell lines at an IC₅₀ value of 40 μM. Flow cytometric analysis revealed costunolide mediated cell cycle arrest at G2/M phase in both the cell types. Western blotting results confirmed the alterations in the expression of cell cycle regulators (cyclin D1, D3, CDK‐4, CDK‐6, p18 INK4c, p21 CIP1/Waf‐1 and p27 KIP1) and apoptosis inducers (caspase‐3 and caspase‐9) upon costunolide treatment in comparison with their expressions in normal breast cell line (MCF‐10A). Costunolide mediated downregulation of positive cell cycle regulators and upregulation of negative cell cycle regulators were related to the induction of apoptosis in cancer cells. The above results were validated with in‐silico results that predicted stable interactions between costunolide and cancer targets. Thus costunolide effectively induced breast cancer cell apoptosis targeting cell cycle regulation, and the compound can be used as an effective herbal therapeutic molecule to treat breast cancer with further explorations. Copyright © 2015 John Wiley & Sons, Ltd.     

益气扶正复方联合依维莫司对三阴性乳腺癌细胞株MDA-MB-468的增殖抑制作用及其对Akt/mTOR信号通路的影响

目的探讨益气扶正复方（简称复方）联合依维莫司对三阴性乳腺癌细胞株MDA-MB-468细胞的增殖抑制作用及Akt/mTOR信号通路的影响。方法高效液相色谱法（HPLC）制备益气扶正复方药物,以MTT比色法分别检测10,20,40,80,160 mg?mL-1复方药物及1,10,100,1000 nmol?L-1依维莫司（Everolimus）12,24,48 h对MDA-MB-468细胞的增殖抑制作用;分别运用IC50浓度的复方40 mg?mL-1与Everolimus 100 nmol?L-1单独及联合干预MDA-MB-468乳腺癌细胞48 h,观察其对细胞增殖的抑制作用,流式细胞仪检测其对细胞周期和凋亡的影响;Western blot法检测其对细胞Akt/mTOR信号通路的影响。结果复方及Everolimus均呈剂量、时间依赖性地抑制了MDA-MB-468乳腺癌细胞增殖,选择IC50浓度的复方40 mg?mL-1与Everolimus 100 nmol?L-1单独及联合干预细胞,联合用药组显著抑制了MDA-MB-468乳腺癌细胞的增殖,同时联合用药组抑制了p-mTOR和p-Akt的活性,提高了PTEN的表达。结论复方与Everolimus均能抑制MDA-MB-468乳腺癌细胞增殖,两药联用效果更为显著,其作用机制可能与复方与依维莫斯联用抑制了p-mTOR和p-Akt的活性,提高了PTEN的表达有关。     

[6]‐Gingerol enhances the cisplatin sensitivity of gastric cancer cells through inhibition of proliferation and invasion via PI3K/AKT signaling pathway

Cisplatin‐based chemotherapy is a widely used chemotherapeutic regimen for gastric cancer; however, drug resistance limits its efficacy. [6]‐Gingerol has been found to exhibit anticancer effects. Here, we aim to explore the potential of [6]‐gingerol in combination with cisplatin as a new regimen for gastric cancer. CCK‐8 assay and colony formation assay were used to determine the effect of [6]‐gingerol in combination with cisplatin on cell viability of gastric cancer cells. Flow cytometry was performed to assess cell cycle distribution. Wound‐healing assay and transwell invasion assay were conducted to examine the migration and invasion abilities. Cell cycle and invasion‐related proteins and mRNAs, as well as PI3K/AKT signaling proteins, were assessed by western blotting and quantitative real‐time polymerase chain reaction. Combination of [6]‐gingerol with cisplatin inhibited cell viability and enhanced cell cycle arrest at G1 phase compared with cisplatin alone. The combination treatment inhibited cell migration and invasion ability and decreased cyclin D1, cyclin A2, matrix metalloproteinase‐9, p‐PI3K, AKT, and p‐AKT protein expressions and increased P21 and P27 mRNA levels. Our study demonstrates that [6]‐gingerol enhances the cisplatin sensitivity of gastric cancer cells and that the mechanisms involve G1 phase arrest, migration and invasion suppression via PI3K/AKT signaling pathway.     

人BMI-1基因真核表达载体构建及其在人乳腺癌细胞系MDA-MB-468细胞中的表达

目的：构建人Bmi-1基因的真核表达载体pcDNA3．1（＋）-Bmi-1,转染人乳腺癌细胞株MDA-MB-468细胞中并检测其表达。方法：RT-PCR检测Bmi．1mRNA在乳腺癌细胞系MCF-7及MDA-MB-468细胞中的表达水平;从MCF-7细胞中提取总RNA,逆转录为cDNA,以cDNA为模板,扩增Bmi-1基因序列,将含有Bmi-1全长编码序列的PCR产物经TA克隆后经PCR、酶切验证,亚克隆入真核表达载体pcDNA3．1（＋）中,构建重组质粒pcDNA3．1（＋）-Bmi-1,转化至大肠杆菌后,酶切、测序鉴定;将重组质粒转染到MDA-MB-468中,48h后RT-PCR检测转染前后Bmi-1mRNA及hTERTmRNA的表达变化。结果：Bmi-1mRNA在MCF-7细胞中表达较高,而在MDA-MB-468细胞中仅适量表达。成功从MCF-7细胞中克隆获得Bmi-1基因并构建真核表达载体。转染后在MDA-MB-468中检测到Bmi-1mRNA表达上调,其过表达上调hTERTmRNA的表达。结论：成功克隆和建立人Bmi-1基因真核表达载体;pcDNA3．1（＋）-Bmi-1能在MDA-MB-468中表达;为进一步研究Bmi-1基因在细胞中的功能奠定了基础。     

Selective Inhibition of Cell Proliferation by Lycopene in MCF‐7 Breast Cancer Cells In vitro: A Proteomic Analysis

Lycopene, a red pigmented carotenoid present in many fruits and vegetables such as tomatoes, has been associated with the reduced risk of breast cancer. This study sought to identify proteins modulated by lycopene during cell proliferation of the breast cancer cell line MCF‐7 to gain an understanding into its mechanism of action. MCF‐7 breast cancer cells and MCF‐10 normal breast cells were treated with 0, 2, 4, 6, 8, and 10 μM of lycopene for 72 h. 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) tetrazolium reduction assay was used to measure cell proliferation and two‐dimensional fluorescence difference gel electrophoresis to assess the changes in protein expression, which were identified using MALDI‐ToF/ToF (matrix‐assisted laser desorption ionization tandem time‐of‐flight) and Mascot database search. MTT and cell proliferation assays showed that lycopene selectively inhibited the growth of MCF‐7 but not MCF‐10 cells. Difference gel electrophoresis analysis revealed that proteins in the MCF‐7 cells respond differently to lycopene compared with the MCF‐10 cells. Lycopene altered the expression levels of proteins such as Cytokeratin 8/18 (CK8/18), CK19 and their post translational status. We have shown that lycopene inhibits cell proliferation in MCF‐7 human breast cancer cells but not in the MCF‐10 mammary epithelial cells. Lycopene was shown to modulate cell cycle proteins such as beta tubulin, CK8/18, CK19 and heat shock proteins. Copyright © 2012 John Wiley & Sons, Ltd.     

葡萄籽提取物原花青素诱导乳腺癌 MCF-7 细胞脱落凋亡

目的 检测葡萄籽提取物原花青素诱导乳腺癌MCF-7细胞脱落凋亡的作用。方法 采用DNA ladder检测及软琼脂集落形成试验方法，观察乳腺癌MCF-7细胞对脱落凋亡的敏感性以及原花青素诱导其脱落凋亡的作用。结果 MCF-7细胞具有抗脱落凋亡的特性，而0．1mmol／L原花青素即可引起悬浮培养的MCF-7细胞凋亡。表现为细胞染色质DNA断裂及软琼脂集落形成受阻。结论 原花青素可诱导乳腺癌MCF-7细胞脱落凋亡。     

疏肝益肾方对人乳腺癌TAM耐药细胞株MCF-7 TAM-R的作用及其机制的研究

目的:研究疏肝益肾方对他莫昔芬耐药乳腺癌细胞MCF-7 TAM-R的作用,并探讨其可能的机制。方法:采用中药血清药理学方法制备大鼠含疏肝益肾方高中低剂量血清、TAM阳性对照血清、空白阴性对照血清,体外培养MCF-7 TAM-R细胞。CCK8法观察各组含药血清对MCF-7 TAM-R细胞株的抑制率,基因芯片检测MCF-7 TAM-R耐药细胞株可能的作用机制。结果:CCK8实验结果显示疏肝益肾方高中低剂量均可不同程度抑制MCF-7 TAM-R细胞株的增殖,且中药高剂量组在48小时抑制作用最强(P0.05)。基因芯片结果显示高剂量疏肝益肾方可以下调MCF-7 TAM-R耐药细胞株MAPK通路、VEGF通路等通路的表达。结论:1疏肝益肾方对TAM耐药乳腺癌细胞MCF-7 TAM-R的增殖有抑制作用。2疏肝益肾方逆转MCF-7 TAM-R细胞他莫昔芬耐药的机制涉及多条通路,可能与抑制MAPK通路、VEGF通路等通路有关。     

清毒饮、养正片影响白血病K562细胞增殖周期、细胞凋亡的实验研究

目的:观察清毒饮、养正片诱导人白血病细胞株K562细胞凋亡及对细胞增殖周期的作用;探索其时效关系,为临床提供选择最佳用药时机的实验基础.方法:制备含清毒饮、养正片药物血清,建立相应的培养体系,加入含药小鼠血清,培养K562细胞株;分别于培养12、24、36、48、72h收集细胞,固定、染色、上流式细胞仪进行细胞周期、细胞凋亡的检测.结果:人白血病K562细胞株存在有自然凋亡,正常小鼠血清无诱导该细胞凋亡的作用;清毒饮、阿糖胞苷具有诱导细胞凋亡的作用,且随着培养时间的延长凋亡率愈加明显.清毒饮对K562细胞周期的影响,还表现出明显的时间依赖性;随着培养时间的延长,当细胞出现明显凋亡时,细胞株S期显著下降,G0/G1期升高,提示清毒饮和清毒加养正合剂都可引起K562细胞株的G0/G1期阻滞,对凋亡的敏感性增强.结论:清毒饮能抑制K562细胞增殖、促进细胞分化、诱导细胞凋亡,提示该中药复方具有从分子水平抗肿瘤细胞增殖的效应,这也是中药复方协同化疗药物治疗白血病在增效减毒方面的关键机制;清毒饮对K562细胞发生细胞毒作用,是通过抑制其细胞周期S期、将其阻滞于G1期,并通过促进K562细胞凋亡实现的,其作用强度与时间呈密切正相关.     

Cytotoxic constituents from Andrographis paniculata induce cell cycle arrest in jurkat cells

Herbal medicines are now attracting attention as potential sources of anticancer agents. Andrographis paniculata is a traditionally used anticancer herb in Indian and Chinese herbal medicine. Phytochemical investigation of the ethanol extract of the aerial parts of this herb resulted in the isolation of 14 compounds including flavonoids and labdane diterpenoids. This is the first isolation of compound 6 from a natural source, and the aerial parts of A. paniculata are a rich source for the molecule andrographolide (9, 1.375%, w/w). The structures of the isolated compounds were established by means of spectral data. The cytotoxic activities of these isolates were evaluated against Jurkat, PC-3, HepG2 and Colon 205 tumor cells, and normal cells PBMCs. The bioactivity assays showed that metabolites 1-4 and 6-8 exhibited moderate cytotoxic activity against Jurkat, PC-3 and Colon 205 cell lines, where compound 6 had IC(50) values of 0.05, 0.07 and 0.05 mm, respectively. Further, among these effective compounds, 3 and 6 selectively blocked the cell cycle progression at G0/G1, while 1, 2, 4, 7 and 8 blocked the same at G2/M phase of the Jurkat cell line. This is the first cell cycle analysis for the above mentioned isolates on the Jurkat cells. Therefore, these plant-derived compounds may play a role in the prevention and/or management of cancer.     

金雀异黄素对人乳腺癌细胞体外生长的抑制作用

目的:研究金雀异黄素(genistein)对人乳腺癌细胞系的体外生长作用及其作用机理。方法:选用人乳腺癌细胞系MCF-7(雌激素受体阳性细胞,ER+)和MDA-MB-231(雌激素受体阴性细胞,ER-)体外培养、MTT比色法、生长曲线和雌激素受体(ER)免疫组化染色等。结果:genistein能明显地抑制MCF-7细胞和MDA-MB-231细胞的体外增殖,而且在一定浓度范围内均呈剂量依赖性,IC50分别是32.5,46.8μmol·L^-1。同时能拮抗外源性雌激素对MCF-7细胞的生长刺激作用,而对MDA-MB-231细胞的生长抑制作用与雌激素的存在与否无关。ER免疫组化染色结果表明,经过30μmol·L^-1 genistein处理的MCF-7细胞,细胞核内的阳性颗粒与对照组相比明显减弱(P<0.001)。结论:genistein能明显抑制MCF-7和MDA-MB-231细胞的体外生长,且呈剂量依赖性;genistein对MCF-7细胞的生长抑制作用是通过ER途径来介导的,而对MDA-MB-231细胞是通过非ER途径来介导的。     

温肾活血法中药对人乳腺癌MCF-7细胞株体内外生长的影响

目的：通过对MCF－7细胞株体内外的研究,揭示温肾活血法中药抑制乳腺癌的作用机理。方法：体外实验用MTT法测定药物血清对细胞的杀伤作用,并用FCM检测各组细胞的细胞周期,体内实验观察药物对体内移植瘤生长的影响。结果：温肾活血中药血清在培养液中浓度为10%、20％和30％时,对MCF－7的体外生长抑制率达22.7%、33.1％和37.4%(P＜0.05）。温肾活血法中药灌饲MCF－7荷瘤裸小鼠后,在剂量为8g/kg、4g/kg、2g/kg时抑瘤率分别为47.5％、44.2％、51.0％。结论：温肾活血法中药可以抑制乳腺癌,其机理可能是通过抑制癌细胞的DNA合成而达到抑制癌细胞的生长。     

大蒜素逆转人乳腺癌MCF-7细胞顺铂耐药性的研究

[目的]探索大蒜素对人乳腺癌MCF-7细胞顺铂耐药性的逆转作用及调控机制.[方法]以对数生长期人乳腺癌耐顺铂MCF-7/DDP细胞为受试细胞,设空白对照组(DMSO)、大蒜素(20μg/mL)单药组、顺铂(6μg/mL)单药组、联合组(大蒜素20μg/mL+顺铂6μg/mL).药物干预48 h后,噻唑蓝(MTT)染色法...     

贝母素甲抑制人乳腺癌细胞MCF-7/TAM增殖及其对细胞凋亡的影响

目的:探讨贝母素甲抑制耐三苯氧胺人乳腺癌细胞MCF-7/TAM的增殖及其机制。方法:采用四甲基偶氮唑蓝(MTT)比色分析法检测贝母素甲作用于MCF-7/TAM细胞后的抑制率;用流式细胞术检测细胞周期和凋亡率;用免疫细胞化学法检测Bcl-2表达变化。结果:贝母素甲对MCF-7/TAM细胞有明显的抑制作用,呈浓度和时间依赖性。作用48h后能诱导细胞凋亡,细胞周期被阻滞于G1期(P0.05)。免疫细胞化学法检测Bcl-2表达减弱(P0.01)。结论:贝母素甲可抑制MCF-7/TAM细胞的增殖,并诱导其凋亡。     

中药方剂R1对耐阿霉素人乳腺癌细胞P糖蛋白表达的影响

免疫细胞化学技术和Western blot分析证实MCF7adr细胞P-糖蛋白(PGP)过量表达，而MCF7细胞无PGP表达。1：60R1(复方R1)和1：90R1处理细胞2小时、3小时均使MCF7adr细胞PGP表达下降，并且与药物作用时间和浓度有关。Northern blot分析示MCFT7adr细胞mdr2 mRNA高表达，而MCFT细胞无表达。1：60R1、1：90R1处理2小时或3小时均使MCF7adr细胞mdr1 RNA表达降低，且随着时间的延长而更加明显。浓度(1：60R1,1：90R1)改变对耐药细胞mdr1 mRNA表达下降的影响程度无明显差异。结果提示R1的逆转作用机理之一可能与其从蛋白质和mRNA水平使耐药细胞PGP表达下降，从而增加细胞内药物聚集量和抗癌药细胞毒性有关。     

Marsdenia tenacissima提取物在体内外水平通过上调14-3-3σ和下调c-myc影响细胞G2/M期周期阻滞

目的：MTE是有抗肿瘤活性的传统中草药提取物。先前的研究揭示了部分MTE抗肿瘤的机制。本研究首次发现MTE能够通过介导14-3-3σ和c-myc从而造成两种人乳腺癌细胞系MDA-MB-231和MCF7的G2/M期细胞周期阻滞。 方法：MTE对G2/M期细胞周期阻滞的影响在人乳腺癌细胞系MDA-MB-231和MCF7。MTT实验用于评价MTE对细胞活力的影响,流式细胞术用于评价MTE对细胞周期的影响。免疫蛋白印迹法和免疫组化用于探究细胞周期关键蛋白在细胞系和肿瘤组织中的表达情况。进行动物实验以探究MTE的抗肿瘤效应。 结果：细胞周期是肿瘤发展的基本过程。细胞周期蛋白在细胞周期和增殖中扮演关键角色。 有一些蛋白质直接或间接调节细胞周期关键蛋白。为了探究肿瘤细胞增殖,我们观察到MTE上调了14-3-3σ,下调了c-myc,并且抑制了G2/M期相关关键蛋白的表达,导致细胞阻滞在有丝分裂期。在MDA-MB-231的小鼠皮下移植瘤模型上,MTE表现出显著的抗肿瘤活性。 结论：MTE通过上调14-3-3σ和下调c-myc造成人乳腺癌细胞MDA-MB-231和MCF7的G2/M期阻滞。