RUNX3基因真核表达载体的构建及其在乳腺癌T47D细胞中的表达

目的:构建真核表达载体pcDNA3.1(+)-RUNX3,并在乳腺癌T47D细胞株中表达。方法:应用基因重组技术和限制性内切酶EcoRI和XhoI酶切,构建并鉴定pcDNA3.1(+)-RUNX3真核表达载体,经脂质体Lipofectamine2000介导质粒转染T47D细胞后应用逆转录-聚合酶链反应(RT-PCR)和Western blot实验,检测RUNX3在T47D细胞中的表达。结果:重组真核表达载体pcDNA3.1(+)-RUNX3经限制性内切酶EcoRI和XhoI酶切,电泳后显示1.3kb的RUNX3目的片段和5.4kb的pcDNA3.1(+)载体片段。测序证实酶切片段与gene bank中登记的RUNX3序列相同,证实pcDNA3.1(+)-RUNX3真核表达载体构建成功。经RT-PCR和Western blot检测,表明转染pcDNA3.1(+)-RUNX3的T47D细胞RUNX3阳性表达。结论:重组真核表达载体构建正确,并建立稳定表达RUNX3的T47D细胞系,从而为后续研究提供有用的细胞研究模型。     

RUNX3基因真核表达载体的构建及其在乳腺癌T47D细胞中的表达

目的：构建真核表达载体pcDNA3.1（＋）-RUNX3,并在乳腺癌T47D细胞株中表达。方法：应用基因重组技术和限制性内切酶EcoRI和XhoI酶切,构建并鉴定pcDNA3.1（＋）-RUNX3真核表达载体,经脂质体Lipofectamine2000介导质粒转染T47D细胞后应用逆转录-聚合酶链反应（RT-PCR）和Western blot实验,检测RUNX3在T47D细胞中的表达。结果：重组真核表达载体pcDNA3.1（＋）-RUNX3经限制性内切酶EcoRI和XhoI酶切,电泳后显示1.3kb的RUNX3目的片段和5.4kb的pcDNA3.1（＋）载体片段。测序证实酶切片段与gene bank中登记的RUNX3序列相同,证实pcDNA3.1（＋）-RUNX3真核表达载体构建成功。经RT-PCR和Western blot检测,表明转染pcDNA3.1（＋）-RUNX3的T47D细胞RUNX3阳性表达。结论：重组真核表达载体构建正确,并建立稳定表达RUNX3的T47D细胞系,从而为后续研究提供有用的细胞研究模型。     

表达白细胞介素-12质粒DNA抗小鼠肝癌皮下移植瘤的作用

目的 探讨瘤内注射mIL-12质粒DNA抗小鼠肝癌皮下移植瘤的作用。方法：构建真核表达质粒载体pDC511mIL-12，ELISA方法检测质粒载体在真核细胞中的表达，淋巴母细胞增殖法检测mIL-12的生物学活性；分别于小鼠肝癌H22皮下移植瘤内直接注射质粒DNA，观察各组小鼠存活时间、肿瘤体积变化及各组小鼠脾脏细胞毒T淋巴细胞(CTL)的活性：注射质粒DNA后1月进行瘤体组织病理学观察：结果：mIL-12基因治疗组与空载体对照组相比，肿瘤生长显著受抑制(F=4．10，P=0．03)，小鼠存活期显著延长(X^2=4．48，P=0．03)．并且小鼠脾细胞CTL杀伤活性增强。质粒DNA瘤内注射1月后，pDC511mIL-12组肿瘤病灶炎性细胞浸润明显，病灶内肿瘤细胞广泛坏死。结论：瘤内注射mIL-12表达质粒DNA可抑制小鼠肝癌皮下移植瘤生长，能提高机体抗肿瘤免疫应答。     

维生素D对乳腺癌细胞及乳腺癌干细胞凋亡的影响

目的:探究维生素D对人乳腺癌细胞及乳腺癌干细胞凋亡的影响。方法:MTT法检测维生素D对乳腺癌SUM159细胞活力的影响;Hoechst33258染色检测维生素D对乳腺癌SUM159细胞凋亡的影响;实时定量PCR法检测维生素D对乳腺癌SUM159细胞凋亡相关分子Bax和Bcl-2 mRNA表达水平的影响;无血清悬浮培养法（serum-free medium,SFM）富集乳腺癌干细胞,显微镜下观察维生素D对乳腺癌干细胞球大小和数量的影响;实时定量PCR法检测维生素D对乳腺癌干细胞凋亡相关分子Bax、Bcl-2 mRNA表达水平的影响。结果:MTT法检测结果显示,维生素D可显著抑制乳腺癌细胞活力,且随着维生素D浓度升高,乳腺癌SUM159细胞活力的下降具有一定的剂量依赖效应,单因素方差分析显示,差异具有统计学意义(P＜0.01);Hoechst33258染色结果显示,维生素D可诱导乳腺癌SUM159细胞发生细胞凋亡形态改变;进一步PCR法检测结果显示,维生素D可显著上调乳腺癌SUM159细胞促凋亡蛋白Bax mRNA的表达,下调抗凋亡蛋白Bcl-2 mRNA的表达,单因素方差分析显示,差异具有统计学意义(P＜0.01)。SFM培养可有效富集乳腺癌干细胞,维生素D干预可明显抑制SFM富集的乳腺癌干细胞球的大小和数量,且与对照组相比,维生素D可显著上调乳腺癌干细胞球Bax mRNA的表达水平,下调Bcl-2 mRNA的表达水平,单因素方差分析显示,差异具有统计学意义(P＜0.01)。结论:维生素D可抑制乳腺癌细胞及乳腺癌干细胞活力,诱导乳腺癌细胞凋亡。     

干扰B7-H4表达通过下调E2F家族相关转录因子抑制乳腺癌细胞的增殖

目的：探讨干扰B7-H4表达对乳腺癌细胞增殖、凋亡、周期以及相关下游分子表达的影响。方法：利用脂质体转染技术分别将特异性靶向B7-H4的siRNA(siB7-H4)及其阴性对照（siNC）转染至对数生长期的乳腺癌T47D和MCF-7细胞,分别命名为T47D-siB7-H4、T47D-siNC、MCF-7-siB7-H4和MCF-7-siNC组。用qPCR法和WB法验证siRNA干扰效果及其对细胞周期分子cyclin D1表达的影响,CCK-8法和FCM分别检测干扰B7-H4表达对T47D和MCF-7细胞增殖、周期和凋亡的影响,qPCR法检测B7-H4干扰对E2F家族相关转录因子表达的影响。结果：成功构建干扰B7-H4表达的乳腺癌T47D和MCF-7细胞。与T47D-siNC和MCF-7-siNC组相比,T47D-siB7-H4和MCF-7-siB7-H4组细胞中B7-H4 mRNA和蛋白表达水平均显著降低、细胞增殖能力显著降低（均P<0.01）,并伴有G1/S期细胞周期阻滞以及cyclin D1表达下调（均P<0.01）,但细胞凋亡率差异无统计学意义（均P>0.05）...     

黄荆子乙酸乙酯提取物对人乳腺癌T47D细胞及其裸鼠移植瘤生长抑制的影响

目的:研究黄荆子乙酸乙酯提取物(EVn-50)对人乳腺癌(T47D)细胞及其裸鼠移植瘤生长抑制的影响.方法:体外培养T47D细胞,溴化标记尿嘧啶(BrdU)掺入法测定细胞核酸合成的抑制作用;平皿克隆形成法测定细胞锚定依赖生长能力的抑制作用;人乳腺癌T47D裸鼠移植瘤模型治疗实验,观察EVn-50在体内对T47D细胞生长抑制作用,HE染色观察乳腺癌组织和细胞形态改变.结果:EVn-50抑制体外培养T47D细胞核酸合成和生长,呈剂量依赖性;EVn-50对裸鼠移植瘤的生长具有显著抑制作用,呈剂量和时间依赖性;EVn-50 80 mg/ kg实验组对移植瘤的瘤重抑制率为51.4% (P<0.001);镜下观察EVn-50 80 mg/ kg实验组肿瘤组织坏死组织较多,细胞异型性较少.结论:黄荆子乙酸乙酯提取物对人乳腺癌有生长抑制作用.     

肝癌移植瘤小鼠髓样抑制细胞比例变化及亚砷酸的调节作用*

目的：探讨髓样抑制细胞（MDSCs）与肿瘤发生、发展的相关性,寻找抑制肿瘤生长的方法。方法：建立H22肝癌细胞昆明鼠皮下移植瘤模型,用共聚焦显微镜观察MDSCs 形态;应用流式细胞仪检测外周血及脾脏中MDSCs 数量在肿瘤生长过程中的变化趋势;给予As2O3 药物干预,即随机分为对照组、As2O3 低剂量组（2mg/kg）、As2O3 高剂量组（4mg/kg）;每周腹腔给药2 次,重复上述测量,统计学分析组间差异;体外细胞培养观察As2O3 对小鼠MDSCs 数量的直接影响。结果：皮下接种肿瘤细胞株后,瘤重逐渐增加,第25天增加至5.67g,外周血和脾脏MDSCs 比例也逐渐增加,分别达20.46% 和9.50% ;对瘤重与外周血和脾脏MDSCs 比例的变化趋势进行相关性分析,相关系数r 值分别为0.95和0.96（t=5.270、5.939,P<0.05）,两者明显呈正相关关系。当用As2O3 药物干预时,外周血低剂量组和高剂量组MDSCs 比例在第28天上升至11.31% 和10.00% ,明显低于阴性对照组（t=3.193、5.486,P<0.05）,且高剂量组MDSCs 比例明显低于低剂量组（t=3.066,P<0.05）;脾脏低剂量组和高剂量组MDSCs 比例在第28天上升至10.90% 和9.04% ,明显低于阴性对照组（t=3.586、5.279,P<0.05）,但高、低剂量组间差异无统计学意义（t=1.298,P>0.05）。 体外实验中,在加入H22肿瘤腹水上清后,培养液中MDSCs 比例于第12天上升至12.67%;加入As2O3 继续培养,MDSCs 的比例于第18天下降至7.44% ,分别与其前一时间点比较,差异有统计学意义（P<0.05）。 结论：荷H22肝癌细胞小鼠体内MDSCs 比例随着肿瘤负荷增大而增加,两者存在正相关性;As2O3 可以降低MDSCs 的比例,缓解肿瘤发生、发展。     

E2F陷阱DNA对人肺癌细胞中stathmin mRNA表达的影响及促进肿瘤细胞凋亡的作用

目的：观察转录因子E2F陷阱DNA对stathmin的表达影响及抑制肿瘤细胞增生情况.方法：采用脂质体LipofectamineTM2000将E2F Decoy ODNs转染入人肺癌A549细胞中,用RT-PCR检测转染细胞中stathmin基因mRNA表达水平变化,通过细胞生长曲线观察转染细胞的增殖能力,Tunel法观察转染细胞凋亡情况.结果：E2F Decoy ODNs被成功转染入肿瘤细胞中,RT-PCR检测结果显示实验组stathmin mRNA表达水平明显低于对照组,而且显著抑制了A549细胞的增殖,空白对照组无明显变化,Tunel凋亡染色可见凋亡细胞.结论：E2F Decoy ODNs能特异性下调stathmin mRNA表达,明显抑制A549细胞的增殖,为肿瘤的基因治疗提供了新的手段.     

表达mIL-21的溶瘤痘苗病毒对小鼠乳腺癌的治疗作用

目的:观察溶瘤痘苗病毒VV△TK△N1L-RFP和VV△TK△N1L-mIL-21对小鼠乳腺癌细胞系JC、TUBO和4T1的体内外治疗效果.方法:采用MTT法比较VV△TK△N1L-RFP和VV△TK△N1 L-mIL-21两种病毒在不同质量浓度下对乳腺癌JC、TUBO和4T1细胞的体外杀伤效果,用TCID50法检测病毒在三株乳腺癌细胞株中的复制能力,用ELISA法检测两种病毒感染细胞后上清液中mIL-21的水平.建立三阴性乳腺癌4T1和Her-2扩增型乳腺癌TUBO细胞移植瘤模型,检测两种病毒的治疗作用.结果:VV△TK△N1L-RFP和VV△TK△N1L-mIL-21两种病毒在乳腺癌JC、TUBO和4T1细胞中均具有复制能力,低剂量的病毒就对乳腺癌细胞产生明显的杀伤效应;VV△TK△N1 L-mIL-21感染的细胞上清中检测到高表达的mIL-21蛋白.在4T1乳腺癌细胞移植瘤模型中,病毒治疗无明显效果(P＞0.05);在TUBO乳腺癌细胞移植瘤模型中,两种病毒均能显著抑制肿瘤生长(P ＜0.05或P＜0.01),延长荷瘤小鼠生存期(P＜0.01).结论:VV△TK△N1L-RFP和VV△TK△N1 L-mIL-21两种病毒在乳腺癌细胞中具有特异性增殖并杀伤肿瘤细胞的能力,在体内两种病毒对Her-2扩增型和三阴性乳腺癌具有不同的治疗效果.     

E2F3在喉鳞状细胞癌中的表达及临床意义

目的：探讨喉鳞癌中E2F3的表达与临床意义,为喉鳞癌的诊断、评估及治疗寻找辅助生物学指标。方法：采用免疫组化方法检测喉鳞癌组织及癌旁正常切缘组织中E2F3表达,结合喉鳞癌各临床参数,用SPSS16.0软件包进行统计分析E2F3表达情况与喉鳞癌各临床特征之间的关系。结果：E2F3在喉鳞癌与癌旁正常切缘中的阳性表达率分别为90.44%（123/136）和27.85%（22/79）,差异具有显著统计学意义（P〈0.001）;E2F3高表达与喉鳞癌患者年龄、临床分期及分型均相关（P〈0.05）。结论：E2F3核表达可能参与喉鳞癌发生发展过程;E2F3浆表达可能贯穿于喉鳞癌发生的整体过程。     

缺氧对乳腺癌和宫颈癌裸鼠移植瘤EGFR表达及细胞凋亡的影响

目的 在乳腺癌、宫颈癌裸鼠成瘤模型中观察缺氧对表皮生长因子受体(EGFR)表达和细胞凋亡的影响。方法 以人乳腺癌MCF-7和宫颈癌HeLa移植裸鼠模型为研究对象,利用激光共聚焦显微镜观察缺氧区程度和EGFR表达情况;利用TUNEL染色观察EGFR表达对缺氧肿瘤细胞凋亡的影响。结果 在乳腺癌MCF-7和宫颈癌HeLa细胞缺氧程度高的区域,EGFR高表达和低表达均存在。此外,与EGFR的低表达肿瘤组织相比,凋亡程度在EGFR高表达肿瘤组织中降低。结论 乳腺癌、宫颈癌细胞缺氧对EGFR表达呈非均一性作用,缺氧诱导EGFR表达与细胞凋亡呈负相关。     

Hyaluronidase reduces human breast cancer xenografts in SCID mice

A hyaluronan-rich environment often correlate with tumor progression. and may be one mechanism for the invasive behavior of malignancies. Eradication of hyaluronan by hyaluronidase administration could reduce tumor aggressiveness and would provide, therefore, a new anti-cancer strategy. Hyaluronan interaction with its CD44 receptor and the resulting signal transduction events may be among the mechanisms for hyaluronan-associated cancer progression. We have shown previously that hyaluronidase treatment of breast cancer cells in vitro not only eradicates hyaluronan but also modifies expression of CD44 variant exons of tumor cells. We now determine if such effects occur in vivo and if it is accompanied by tumor regression. SCID mice bearing xenografts of human breast carcinomas were given intravenous hyaluronidase. Tumor volumes decreased 50% in 4 days. Tumor sections showed decreased hyaluronan. Intensity of staining for CD44s was not affected, whereas staining for specific CD44 variant exon isoforms was greatly reduced in residual tumors. Necrosis was not evident. Hyaluronidase, used previously as an adjunct in cancer treatment, presumably to enhance penetration of chemotherapeutic drugs, may itself have intrinsic anti-cancer activity. Removing peritumor hyaluronan appears to cause an irreversible change in tumor metabolism. Continuous hyaluronan binding to CD44 variant exon isoforms may also be required to stabilize inherently unstable isoforms that participate perhaps in tumor progression. Further investigation is required to confirm a cause and effect relationship between loss of hyaluronan, changes in CD44 variant exon expression and tumor reduction. If confirmed, hyaluronidase may provide a new class of anti-cancer therapeutics and one without toxic side effects.     

组蛋白酶和c-erbB-2在乳腺癌中的表达

目的探讨乳腺癌病人c-erbB．2和cath-D表达与临床病理及预后的关系。方法通过免疫组化法，检测128例乳腺癌病人的c-erbB-2和cath-D的表达。结果cath-D和c-erbB-2表达与肿块大小、淋巴结转移显著相关（P〈0．0001）。c-erbB-2表达比不表达病人预后差（P=0．01）。结论c-erbB-2阳性表达和cath-D阳性表达者，恶性程度高，易转移、预后差。     

Antitumor effects of artesunate on human breast carcinoma MCF-7 cells and IGF-IR expression in nude mice xenografts

Purpose： The objective of this study was to investigate the anti-tumor effects and analyze the mechanism of artesunate （ART） action on breast cancer in vivo using tumor transplanted nude mice. Methods： The human breast tumor cell line MCF-7 was transplanted into nude mice, and the animals were treated with various doses of ART alone or in combination with cyclophosphamide （CTX） or normal saline （NS）. The tumor inhibitory effects were observed and compared, and the ultrastructural morphology of the transplanted tumor cells was observed by electron microscopy. The apoptosis rates and cell cycle status were detected by flow cytometry （FCM）. The expression of apoptosis-related proteins p53, Bcl-2, Bax and Caspase-3 were detected by immunohistochemistry and IGF-IR was detected by western blot. The expression correlation for these proteins was also analyzed. Results： The tumor inhibition rates in the low dose ART group, high dose ART group, CTX group and combined drug therapy group were （24.39±10.20）%, （40.24±7.02）%, （57.01±5.84）% and （68.29±5.1）%, respectively. The cell cycle was arrested in phase G0/Gt after treatment with ART. The expression of Bcl-2 was significantly reduced, and the expression levels of Bax and Caspase-3 were significantly increased in the ART group compared to the negative control saline group. There was no significant difference detected in p53 expression. The Bcl-2 level was negatively related to Bax and Caspase-3. The western blotting results showed IGF-IR downregulation. Conclusions： ART inhibits the growth of MCF-7 breast tumor cell xenografts in nude mice. The anti-tumor mechanism of ART for human breast carcinoma in nude mice might be correlated with the alteration of apoptosis related protein expression, which may further induce apoptosis and inhibit cell proliferation.     

塞来昔布抑制人类三阴性乳腺癌裸鼠移植瘤生长的实验研究

 【摘要】　目的　探讨塞来昔布（celecoxib）对人类三阴性乳腺癌（TNBC）肿瘤生长及细胞凋亡的影响。方法　32只裸鼠于背部皮下接种人类TNBC细胞株MDA-MB-231,随机分为空白对照组及低、中、高剂量塞来昔布组（25、50、100 mg?kg-1?d-1）。实验结束后,留取移植瘤标本,观察用药前后裸鼠肿瘤体积的变化;流式细胞术（FCM）检测肿瘤细胞凋亡率;免疫组织化学法检测NF-κB p65和p50分子的表达;Western blot法检测凋亡相关分子Caspase-3、Survivin蛋白的表达。结果　塞来昔布治疗组肿瘤体积较对照组均明显减小。中、高剂量塞来昔布治疗组凋亡率分别为（13.58±3.16）％、（21.91±4.75）％,与对照组的（3.15±1.73）％相比差异有统计学意义（t＝6.736,12.151,均P＜0.05）,塞来昔布低、中、高剂量组p65表达阳性率分别为79.3 %、46.7 %、23.9 %,与对照组（89.7 %）相比差异有统计学意义（χ2＝3.312,10.785,15.900,均P＜0.05）。Western blot结果显示,塞来昔布治疗后肿瘤组织中Caspase-3蛋白出现了裂解片段,并且随药物浓度增加,裂解片段表达量逐渐增加。Survivin蛋白随药物浓度增加表达逐渐下调。结论　塞来昔布可以诱导TNBC裸鼠移植瘤细胞凋亡,抑制肿瘤生长,其抗肿瘤作用机制可能部分与抑制p65分子以及下调Survivin蛋白表达有关。     

ECM1-pEGFP-N2 真核表达载体的构建及其在人乳腺癌细胞系MCF-7中的表达

目的构建细胞外基质蛋白1基因（ECM1）的真核表达载体ECM1-pEGFP-N2,检测其在人乳腺癌细胞系MCF-7中表达。方法采用PCR方法,以ECMleDNA为模板,扩增出ECM1基因,用Bg1 Ⅱ和KpnⅠ双酶切ECM1基因和pEGFP-N2载体,连接酶切目的片段,转化大肠杆菌DH5,筛选阳性克隆酶切、测序鉴定;利用脂质体介导的转染技术转染MCF-7细胞,荧光显微镜检测报告基因表达产物EGFP,免疫组化检测ECM1蛋白表达。结果利用PCR克隆出约1．6kb的ECM1基因;PCR鉴定、酶切鉴定及测序结果证实成功构建ECM1-pEGFP-N2真核表达载体;转染MCF-7细胞后,可在细胞内观察到报告基因产生的绿色荧光,用免疫组化方法可检测到ECM1蛋白。结论成功构建了ECM1-pEGFP-N2真核表达载体,并在MCF-7细胞中表达,为进一步研究ECM1的功能奠定了基础。     

Anticancer effects of wogonin in both estrogen receptor-positive and -negative human breast cancer cell lines in vitro and in nude mice xenografts

Wogonin is a plant monoflavonoid which has been reported to inhibit cell growth and/or induce apoptosis in various tumors. Herein, we investigated the in vitro and in vivo anticancer effects and associated mechanisms of wogonin in human breast cancer. Effects of wogonin were examined in estrogen receptor (ER)-positive and -negative human breast cancer cells in culture for proliferation, cell cycle progression, and apoptosis. The in vivo effect of oral wogonin was examined on tumor xenograft growth in athymic nude mice. The molecular changes associated with the biological effects of wogonin were analyzed by immunoblotting. Cell growth was attenuated by wogonin (50-200 microM), independently of its ER status, in a time- and concentration-dependent manner. Apoptosis was enhanced and accompanied by upregulation of PARP and Caspase 3 cleavages as well as proapoptotic Bax protein. Akt activity was suppressed and reduced phosphorylation of its substrates, GSK-3beta and p27, was observed. Suppression of Cyclin D1 expression suggested the downregulation of the Akt-mediated canonical Wnt signaling pathway. ER expression was downregulated in ER-positive cells, while c-ErbB2 expression and its activity were suppressed in ER-negative SK-BR-3 cells. Wogonin feeding to mice showed inhibition of tumor growth of T47D and MDA-MB-231 xenografts by up to 88% without any toxicity after 4 weeks of treatment. As wogonin was effective both in vitro and in vivo, our novel findings open the possibility of wogonin as an effective therapeutic and/or chemopreventive agent against both ER-positive and -negative breast cancers, particularly against the more aggressive and hormonal therapy-resistant ER-negative types.     

Chemosensitivity of human gastrointestinal and breast cancer xenografts in nude mice

Experimental chemotherapies for 15 human cancers xenografted into nude mice were performed using 14 anticancer agents including 6 drugs in clinical use. Treatment with each single agent was performed for every cancer line using the maximum tolerated dose through continuous daily (antimetabolites) or intermittent (cytocidal agents) schedules. Effectiveness of each drug was evaluated by inhibition rate (IR) calculated from mean tumor weights of both treated and untreated groups. Response to a treatment was judged as effective when the IR was higher than 58%. Response rate of each drug was as follows; MMC was 67%, UFT 67%, CPA 47%, FT-207 40%, ACNU 33%, ADR 27%, SOAz 87%, 5'-DFUR 80%, MXT 20%, Leakadine 17%, M-83 17%, CAM 0% and GANU 0%. Generally, the experimental results for each drug on the xenografts was in good accordance with the known clinical effect of each drug on the same type of cancer. On the other hand, individual cancer xenografts showed considerable differences in chemosensitivity. Some tumors were sensitive to a majority of the drugs, whereas some were resistant to many of them. Each cancer line seemed to retain individuality in its spectrum of chemosensitivity irrespective of whether it originated from the same organ or whether it was of similar histologic type. This fact suggests the necessity of selecting drugs effective to the individual tumor when considering a patients chemotherapy regime.     

红景天对裸鼠乳腺癌移植瘤的影响

背景与目的：体内外的肿瘤研究显示红景天具有一定的抗肿瘤作用，本文探讨红景天对于乳腺癌移植瘤的生长的抑制作用及其可能的机制。方法：以人乳腺癌MDA—MB-435细胞的裸鼠移植瘤模型作为研究对象，采用免疫组织化学方法，从转移瘤内的肿瘤细胞增殖活性方面，探讨红景天对乳腺癌移植瘤的作用。结果：与生理盐水对照组相比，红景天治疗组的移植瘤体积有所缩小，但未达到统计学意义（99．95mm^3比174．60mm^3，P=0．535）；红景天治疗后移植瘤内乳腺癌细胞增殖指标Ki-67染色比例、染色强度降低，其综合评价指数H-分数均值明显降低（152．8比86，P=0．014）；移植瘤内增殖指标PCNA的染色强度和比例的综合评价指数H-分数均值有所降低，但未达到统计学意义（242比210，P=0．221）。结论：红景天的体内抗癌机制可能部分通过抑制肿瘤的增殖活性而实现。