高转移人卵巢癌细胞系及其母系多基因表达研究

为研究高转移人卵巢癌细胞系ＨＯ８９１０ＰＭ及其母系ＨＯ８９１０多基因表达情况及其彼此关系,采用ＳＰ免疫组化染色方法,观察了９种基因产物的表达。结果显示,除ｂａｘ外,其余８种基因产物在２株细胞均呈不同程度的阳性表达。在ＨＯ８９１０ＰＭ细胞系中,以ｐ５３、ＣｙｃｌｉｎＤ１、ＣＤ４４Ｖ６、ＥＧＦＲ的表达强度强于母系;而ｐ１６、ｎｍ２３表达强度则较母系弱。２株细胞ｃｅｒｂＢ２、ｂｃｌ２表达无明显不同。结果表明,ＨＯ８９１０ＰＭ是一株较母系ＨＯ８９１０更具侵袭和转移生长潜能的细胞株。同时也证实肿瘤的发生、浸润和转移是多基因参于、多阶段协同作用的结果     

斑蝥素抑制人高转移卵巢癌细胞HO-8910PM侵袭转移的体外实验研究

背景与目的:斑蝥素在治疗癌症方面显示出其独特的疗效,已有较多文献证实核因子鄄κB(nuclearfactor鄄kappaB,NF鄄资B)与肿瘤侵袭转移关系密切。本研究旨在观察斑蝥素对人高转移卵巢癌细胞HO鄄8910PM转移相关能力的影响,并探讨其作用机理。方法:MTT法及细胞粘附人工重组基底膜实验检测斑蝥素对HO鄄8910PM细胞的细胞毒作用及粘附能力的影响;用Transwell小室法检测斑蝥素对HO鄄8910PM细胞侵袭能力和趋化运动能力的影响;Westernblot法分析斑蝥素对HO鄄8910PM细胞中NF鄄κB和血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)的影响。结果:20μmol/L的斑蝥素作用6h对HO鄄8910PM细胞抑制率及体外侵袭、趋化运动和粘附的抑制率分别为(8.4±2.2)%及(38.8±1.7)%、(40.3±5.6)%和(55.1±6.7)%。20μmol/L斑蝥素能明显下调HO鄄8910PM细胞中NF鄄κB和VEGF的表达。结论:斑蝥素能抑制HO鄄8910PM细胞的侵袭、运动和粘附能力。斑蝥素抗肿瘤侵袭转移的作用机制与NF鄄κB和VEGF蛋白的表达下调有关。     

DOC-2对卵巢癌细胞HO-8910致瘤力的影响

背景与目的：作为近年发现的新的肿瘤抑制基因，DOC-2的作用机制还不完全清楚。本实验的目的在于观察DOC-2转染后对卵巢癌细胞系HO-8910在克隆形成率、细胞周期、裸鼠致瘤能力等方面的影响，并对其作用机制进行初步探讨。方法：实验分3组：卵巢癌细胞系HO-8910（无DOC-2基因的表达）、8910-P93（经转染并表达DOC-2基因）、8910-pcDNA3．1（转染空载体pcDNA3．1），首先通过软琼脂克隆形成实验比较3组细胞克隆形成率的差异，之后利用流式细胞仪观察其细胞周期的变化，最后用裸鼠荷瘤实验进一步验证DOC-2对肿瘤细胞致瘤能力的影响。结果：卵巢癌细胞系HO-8910在转染DOC-2后其克隆形成率明显降低，与转染前差异明显（P〈0．05），同时G．和G，期细胞明显增多而S期细胞明显减少，移植瘤裸鼠荷瘤实验显示HO-8910-P93细胞在裸鼠体内生长缓慢，肿瘤体积及重量均明显低于对照组（P〈0．05）。结论：DOC-2基因能明显抑制卵巢癌细胞系HO-8910的致瘤力。     

Establishment of a highly metastatic human ovarian cancer cell line (HO-8910PM) and its characterization.

To establish a highly metastatic human ovarian cancer cell line and to study its characteristics tissue from the tumor mass of a nude mouse of 7th subtransplantation of the highly metastasizing human ovarian cancer model (NSMO) was cultured in vitro and the cell line HO-8910PM was established. The cell line grew well through 87 passages and the mitotic index, chromosome analysis, morphology under electron microscope and some oncoprotein expression were studied. The cell doubling time was 34.5 h and the mitotic index was 44.3%. The cells were all of epithelial type and most of them were of polygonal shape. Electron microscopic examination showed malignant nuclei with enlarged nucleoli and abundant microvilli. The plating efficiency in soft agar was 31.2%. The cell agglutination appeared in 4 ug/ml PHA. Chromosomal analysis revealed a mode of 54 per cell. The DNA index was 1.57 measured by FCM. Both of them showed hyperdiploid. Positive ER and PR granules were found in the cells. After hetero-transplantation of the cells into three nude mice all of the latter showed tumor growth with metastasis in lungs or lymph nodes. Eight of the nine kinds of oncoprotein detected by immnohistochemical method were found in the cells. The detection for mycoplasma showed negative. After storage in liquid nitrogen cell growth was stable. The cell line HO-8910PM can meet the criteria for the establishment cell lines. This cell line and NSMO model would be very useful in study of the mechanism of cancer metastasis in identifying various cellular factors regulating local and distant metastasis and also in establishing a rational approach for searching after anti-metastatic agents.     

Silencing of IQGAP1 by shRNA inhibits the invasion of ovarian carcinoma HO-8910PM cells in vitro

Background

IQGAP1 is a scaffolding protein and overexpressed in many human tumors, including ovarian cancer. However, the contribution of IQGAP1 to invasive properties of ovarian cancer cells remains unknown. Here, we investigated the effect of IQGAP1-specific short hairpin RNA (shRNA) expressing plasmids on metastatic potential of ovarian cancer HO-8910PM cells.

Methods

We used RT-PCR and Western blot analysis to characterize expression of IQGAP1 in three human ovarian cancer-derived cell lines SK-OV-3, HO-8910 and HO-8910PM. We then determined whether expression of endogenous IQGAP1 correlated with invasive and migratory ability by using an in vitro Matrigel assay and cell migration assay. We further knocked down IQGAP1 using shRNA expressing plasmids controlled by U1 promoter in HO-8910PM cells and examined the proliferation activity, invasive and migration potential of IQGAP1 shRNA transfectants using MTT assay, in vitro Matrigel-coated invasion assay and migration assay.

Results

IQGAP1 expression level seemed to be closely associated with the enhanced invasion and migration in ovarian cancer cell lines. Levels of both IQGAP1 mRNA and protein were significantly reduced in HO-8910PM cells transfected with plasmid-based IQGAP1-specific shRNAs. RNAi-mediated knockdown of IQGAP1 expression in HO-8910PM cells resulted in a significant decrease in cell invasion and migration.

Conclusion

Our findings support the hypothesis that IQGAP1 promotes tumor progression and identify IQGAP1 as a potential therapeutic strategy for ovarian cancer and some other tumors with over-expression of the IQGAP1 gene.     

高低转移人卵巢癌细胞系基因表达谱差异

目的 用基因芯片技术研究高低转移人卵巢癌细胞系（HO－8910PM和HO－8910）基因表达谱差异,筛选与转移相关的基因。方法 分别抽提高低转移人卵巢癌细胞和对照正常卵巢上皮的总RNA并纯化mRNA;分别将等量的mRNA逆转录合成以图像,用软件对扫描图像进行数字化处理和分析。结果 HO－8910细胞与正常卵巢上皮比较差异3倍以上共有355个基因;HO－8910PM细胞与正常卵巢上皮比较差异3倍以上共有323个基因。HO－8910PM与母系HO－8910比较差异2倍以上共有163个基因,差异3倍以上共有21个基因。结论 两株人卵巢癌细胞与正常卵巢上皮细胞基因表达谱存在差异,提示这些基因与卵巢癌的发生和发展有关;HO－8910PM与HO－8910比较存在差异的基因可能与高转移特性相关。     

The gene expression profile of highly metastatic human ovarian cancer cell line by gene chip

In this paper, gene chip technique was used to analyze the difference of gene expression patterns in highly metastatic human ovarian tumor cell line HO-8910PM and in normal ovarian epithelial cells to explore the tumor-associated gene-cluster and its function in the process of occurrence an development of ovarian carcinoma. It will be helpful to comprehensively understand the molecular mechanism of cell transformation, to provide the molecular markers and target genes for clinical diagnosis a…     

三种腺苷类似物抑制人高转移卵巢癌细胞侵袭的实验研究

背景与目的:腺苷作用于细胞信号转导系统,可抑制磷脂酰肌醇4-激酶活性、升高腺苷酸环化酶活性和细胞内cAMP水平、抑制血小板肌动蛋白聚合等。腺苷类似物有上述腺苷的生物活性,且不易为腺苷脱氨酶所降解,具有相对较长的生物半衰期。本研究拟观察2-氯腺苷、2-氯脱氧腺苷、2'-脱氧腺苷对人高转移卵巢癌细胞HO-8910PM体外侵袭的抑制作用。方法:以3种腺苷类似物处理HO-8910PM朱峰,等.三种腺苷类似物抑制人细胞、以5-氟尿嘧啶为细胞敏感对照,用台盼蓝拒染法观察药物对细胞的毒性效应;以人工重组基底膜观察细胞的侵袭、粘附和运动能力;以明胶酶显影法观察细胞基质金属蛋白酶-9(matrixmetalloproteinase-9,MMP-9)的分泌及活性;以RT-PCR检测细胞mta1mRNA、nm23H1mRNA表达。结果:2-氯腺苷和2-氯脱氧腺苷处理高转移卵巢癌细胞72h的IC50值分别为5.80μmol/L和2.61μmol/L,2'-脱氧腺苷对该细胞无明显抑制(对细胞的IC50值大于100μmol/L);6.0μmol/L的2-氯腺苷和2-氯脱氧腺苷对细胞侵袭的抑制率分别为(42.5±1.5)%(与对照组比较,P<0.01)和(9.9±0.5)%(P<0.05);对细胞运动的抑制率分别为(36.9±2.1)%(P<0.01)和(17.1±0.4)%(P<0.05);对细胞粘附的抑制率分别为(32.2±2.3)%(P<0.01)和(19.5±3.1)%(P<0.05)。而2'-脱氧腺     

吉西他滨联合放射对人高转移卵巢癌细胞的体外实验研究

Objective  

The aim of the study was to investigate the mechanism of gemcitabine (GEM) combination with radiation on the high metastasis human ovarian cancer cell line (HO-8910PM).     

三氧化二砷联合抗坏血酸对高转移性卵巢癌细胞系HO-8910PM的抗肿瘤实验研究

[目的]在高转移性上皮性卵巢癌细胞株HO-8910PM中观察AS2O3联合抗坏血酸（VitaminC）的抗肿瘤效应。[方法]本研究以高转移性上皮性卵巢癌细胞株HO-8910PM为研究对象,以MTT药敏实验、流式细胞仪以及Western-blot方法检测AS2O3和VitaminC单药及联合的抗肿瘤效应及其机制。[结果]AS2O3和VitaminC单药对HO-8910PM细胞株均具有剂量依赖性的生长抑制作用。AS2O3联合VitaminC后具有明显的协同抗肿瘤效应,并且出现S期阻滞效应。Western-blot结果显示。AS2O3和VitaminC联合作用后,凋亡抑制蛋白bcl-2和凋亡促进蛋白bax分别进一步表达下调和上调。[结论]对高转移性的上皮性卵巢癌细胞株,VitaminC和AS2O3单药均具较好的抗肿瘤效应,VitaminC对AS2O3有较好的化疗增敏效应,两者的联合应用值得在卵巢癌方面进一步研究探讨。     

肿瘤抑制基因DOC-2真核表达载体的构建及在卵巢癌细胞HO-8910中的表达鉴定

目的构建肿瘤抑制基因DOC-2的真核表达载体pCDNA3.1-p93,将其转入人卵巢癌细胞系HO-8910中,对其基因表达进行相关检测,为进一步研究DOC-2的功能奠定基础。方法利用XhoI酶切含有p93cDNA的质粒得到p93cDNA基因片段,将其连接入真核表达载体pCDNA3.1,并通过酶切鉴定。用脂质体介导法将真核表达载体pCDNA3.1-p93转染HO-8910,通过G418筛选稳定表达克隆;用免疫组化法观察人DOC-2蛋白在HO-8910中的表达。结果构建了DOC-2的真核表达载体pCDNA3.1-p93,并通过酶切鉴定。免疫细胞化学结果显示pIRES2-EGFP-p93成功转入HO-8910中。结论成功构建了真核表达载体pCDNA3.1-p93并在HO-8910中得到稳定表达,为研究DOC-2蛋白的功能奠定了基础。     

熊果酸对卵巢癌细胞转移的抑制作用

目的 熊果酸(UA)对人卵巢癌细胞株HO-8910PM黏附、侵袭及趋化运动的影响,并探讨其可能的作用机制。方法 采用MTT法方法检测熊果酸对HO-8910PM细胞黏附能力的影响;Transwell小室进行人工重组基底膜侵袭实验检测熊果酸对HO-8910PM细胞侵袭及运动的影响;采用RT-PCR和Western blot方法检测熊果酸对HO-8910PM细胞中MMP-2 mRNA、MMP-9 mRNA和蛋白的表达的影响。结果 在黏附试验中,不同浓度熊果酸作用细胞24h后,抑制率分别为44.03%、46.62%和55.11%,与对照组比较具有统计学意义(P＜0.05)。不同浓度的熊果酸在体外作用24h后可以显著抑制HO-8910PM细胞的侵袭能力,穿膜细胞数与对照组比较具有统计学意义(P＜0.01)。熊果酸处理后细胞趋化运动能力降低与对照组比较差异有统计学意义(P＜0.05)。不同浓度熊果酸作用24小时后,HO-8910PM细胞MMP-2 mRNA、MMP-9 mRNA表达量明显低于正常对照组(P＜0.05),Western blot结果显示:HO-8910PM细胞MMP-2、MMP-9蛋白表达量受到明显抑制(P＜0.05)。结论 熊果酸抑制人卵巢癌细胞株HO-8910PM黏附、侵袭和转移的生物学行为,其作用机制可能与熊果酸显著抑制MMP-2、MMP-9表达水平有密切关系。     

大黄素、芹菜素抑制人卵巢癌细胞侵袭的体外实验研究

背景与目的:大黄素抑制酪氨酸蛋白激酶、酪蛋白激酶2的活性,抑制I-κB降解;芹菜素抑制丝裂原活化蛋白激酶、PI3K的活性。大黄素、芹菜素是否能抑制高恶性度肿瘤侵袭与转移的研究还未见报道,本研究选用大黄素、芹菜素,观察其对人卵巢癌细胞体外侵袭的作用。方法:台盼蓝活细胞拒染法观察药物对人卵巢癌细胞生长、增殖的影响;以人工重组基底膜(Matrigel)体外侵袭实验观察药物对细胞体外侵袭、粘附、运动能力的影响;SDS-聚丙烯酰胺凝胶电泳法观察对Ⅳ型胶原酶分泌及活性的影响。结果:大黄素及芹菜素均抑制HO-8910PM细胞的生长、增殖,其48h的IC50分别为(35.30±3.50)μmol/L和(28.92±2.60)μmol/L。大黄素有效抑制HO-8910PM细胞体外侵袭、粘附、运动,在40μmol/L时,抑制率分别为(45.31±3.10)%、(25.42±1.70)%和(41.59±1.90)%;大黄素抑制基质金属蛋白酶-9(MMP-9)分泌,但不能直接抑制其活性。芹菜素能抑制细胞粘附、运动,在40μmol/L时,抑制率分别为(30.80±3.00)%和(29.04±1.70)%,但抑制细胞体外侵袭作用不显著,仅为(12.08±0.50)%,且不能抑制MMP-9分泌也不能直接抑制其活性。结论:大黄素、芹菜素对人卵巢癌HO-8910PM细胞均有一定的毒性,而大黄素更具有成为抗肿瘤侵袭药物的潜力。     

P16 GENE EXPRESSION IN OVARIAN EPITHELIAL CYSTADENOCARCINOMA

Itiswellknownthatc-oncogeneovereXPressionaswellasantioncogeneabsenceorinactivationplayaveryimportantroleincarcinogenesis.P16gene(orMTSI,Multipletumorsuppresser1)hasbeenwidelyanalyzedinvariousprimarytumors,suchasmelanoma,neuroblastomaandtumorsinkidney,esophagus,stomach,bladder,breastandpancreas.Theresultsfromdifferentresearchshowedahigh-frequentP16genemutationandabsence.'-ToexplaintherelationshipbetweenP16geneandovarian'cancer,wehadanalyzedP16expressioninhumanovarianpoorlydifferentiatedcyst…     

The inhibiting effects of Laggera alata flavone on human ovarian cancer HO-8910 cells proliferation and its mechanism in vitro

The purpose of this study was to investigate the effect of Laggera alata flavonen （LAF） on the inhibit- ing effect of human ovarian cancer HO-8910 cells proliferation and its possible mechanism in vitro. Methods： Human ovarian cancer HO-8910 cells were cultured in vitro. Inhibitory effect of LAF on the viability of HO-8910 cells was evaluated by the MTT assay. Apoptotic effect of different concentrations of LAF on HO-8910 cells was assessed by AO/EB staining and FCM with propidium iodide （PI） staining. Expression of proteins related to apoptosis was analyzed by Western blot. Results： LAF significantly inhibited the viability of HO-8910 cells proliferation in a dose-dependent and time-dependent manner, there were statistical significance compared with NS group （P 〈 0.05）, and the ICso was 4.28 pg/mL for 48 h. The cells treated with LAF showed typical morphological change and apoptotic rate increased by FCM in a dose-dependent, and there was notable dif- ference compared with NS group （P 〈 0.05）. Western blot showed that expression of Fas, caspase-8, tBid and Cyto-c proteins were up-regulated after treatment with LAF for 48 h in a concentration dependent. Conclusion： LAF could inhibit HO-8910 cells proliferation and induce apoptosis, which may be through the pathway of death receptor in vitro.     

亚毒性浓度顺铂联合紫花牡荆素体外诱导人卵巢癌细胞调亡(英文)

Objective: The aim of the study was to investigate the effect of Casticin (CAS) combination with Cisplatin (DDP) in sub-toxic concentration on apoptosis of human ovarian cancer HO-8910 cells in vitro and unravel the associated mechanisms. Methods: Human ovarian cancer HO-8910 cells were cultured in vitro. The inhibitory effect of CAS combination with DDP in sub-toxic concentration on viability of human ovarian cancer HO-8910 cells was evaluated by the MTT assay. Morphological changes of cell apoptosis were detected by Hoechst 33258 staining assay. Cell apoptosis rate was analyzed by flow cytometry. The protein expression level was analyzed by Western blot. Results: CAS in sub-toxic concentration and DDP in sub-toxic concentration could slightly inhibit Human ovarian cancer HO-8910 cells, but CAS combination with DDP in sub-toxic concentration significantly inhibited the growth of HO-8910 cells, and growth inhibition rate was increased drastically compared with the control group (P﹤0.01), and the inhibiting effect showed synergistic action. Human ovarian cancer HO-8910 cells showed the typical morphological changes of apoptosis and apoptosis rate markedly increased when they were exposed to CAS combination with DDP in sub-toxic concentration for 48 h. Western blot showed that the expression of bcl-2 protein was down-regulated and protein level of caspase-3 was activated by CAS combination with DDP in sub-toxic concentration. Conclusion: CAS combination with DDP in sub-toxic concentration could inhibit the cells growth and lead to cell apoptosis in human ovarian cancer HO-8910 cells. And the down-regulation of bcl-2 protein expression and activation of caspase-3 protein might contribute to CAS combination with DDP in sub-toxic concentration in human cancer HO-8910 cells.     

紫杉醇作用卵巢癌细胞系HO-8910后CYP1B1 mRNA及蛋白表达差异的研究

背景与目的:用紫杉醇(paclitaxel,PTX)对卵巢癌细胞系HO-8910进行体外化疗后,观察CYP1B1表达的变化,以期探讨CYP1B1基因表达与肿瘤细胞耐药的关系. 材料与方法:以不同浓度PTX(分别为30、15、7.5、3.75、1.88、0.94、0.47 μg/mi)处理H0-8910细胞.采用四甲基偶氮唑蓝(MTT)比色法检测PTX对HO-8910细胞体外生长的抑制作用,实验同时设只加培养液的对照组.以5 μg/ml PTX分别处理HO-8910细胞24 h、48 h、72 h和50#g/ml PTX处理细胞24 h后,用RT-PCR技术检测存活的卵巢癌细胞中CYP1B1 mRNA的表达水平,用Western blot检测细胞CYP1B1蛋白表达.结果:PTX能抑制HO-8910细胞生长,7种不同浓度的PTX作用72 h后,细胞的抑制率分别为89.10%、76.82%、67.39%、57.27%、46.21%、37.02%、17.56%,随着药物浓度的下降,其抑制率明显降低,各浓度组细胞抑制率间的差异具有统计学意义(P<0.05).经PTX处理后存活的HO-8910细胞中CYP1B1 mRNA及蛋白的表达量增加,高于对照组;5 μg/ml PTX处理HO-8910细胞48 h、72 h和50 μg/ml的PTX处理24 h组,CYP1B1蛋白的表达量高于5 μg/ml PTX处理24 h组(P<0.05).结论:CYP1B1在卵巢癌细胞系中呈高表达,CYP1B1基因在卵巢癌细胞系H0-8910体外PTX化疗中起抑制作用.     

p16基因在人卵巢上皮癌细胞系中的缺失分析研究

目的：了解新型抑癌基因ｐ１６在人卵巢上皮癌细胞系中的变异情况,为认识卵巢上皮癌的形成和发展依据。方法：应用ＰＣＲ扩增、ｍＲＮＡ原位杂交和免疫细胞化学方法,对５种人卵巢上皮癌细胞系ＣＡＯＶ３、ＯＶＣＡＲ３、ＡＯ、ＨＯ－８９１０及ＨＯ－８９１０ＰＭ进行分析。结果：５种人卵巢上皮癌细胞系中只有ＣＡＯＶ３（２０％）显示ｐ１６基因纯合性缺失,ＣＡＯＶ３细胞亦无ｐ１６基因ｍＲＮＡ及蛋白表达。ＯＶＣＡＲ３、Ｈ０     

Inhibition of CD147 gene expression via RNA interference reduces tumor cell invasion, tumorigenicity and increases chemosensitivity to paclitaxel in HO-8910pm cells

Overexpression of extracellular matrix metalloproteinase inducer (EMMPRIN or CD147), a member of the immunoglobulin family and a glycoprotein enriched on the surface of tumor cells, promotes invasion, metastasis, growth and survival of malignant cells, and confers resistance to some chemotherapeutic drugs. Here, we used a human U6 promoter-driven DNA template approach to induce short hairpin RNA (shRNA)-triggered RNA interference (RNAi) to block CD147 gene expression in the human ovarian cancer cell line HO-8910pm. Knockdown of CD147 by shRNA resulted in decrease of the HO-8910pm invasion activity in vitro and tumorigenicity in nude mice. The suppression of CD147 expression also sensitized cells to be more sensitive to paclitaxel. These results suggested that CD147 was an ovarian cancer-related gene and CD147 might be a potential target for therapeutic anti-cancer drugs.     

枸杞原汁、枸杞多糖诱导人正常肝细胞L-O2及卵巢癌细胞株SKOV3、HO8910凋亡的实验研究

目的:对比研究枸杞原汁、枸杞多糖对人正常肝细胞L-O2及人卵巢癌细胞株SKOV3、HO8910的生长抑制,及诱导凋亡的作用及其机制。方法:枸杞原汁、枸杞多糖作用L-O2、SKOV3、HO8910,用MTT法检测细胞生长抑制率,流式细胞仪检测细胞凋亡率并分析细胞周期分布的变化。结果:枸杞原汁组:L-O2、SKOV3、HO8910生长抑制率分别为-58%,-49%,-84%;L-O2、HO8910凋亡细胞含量明显少于空白对照组,正常细胞数明显多于空白对照组;枸杞原汁对L-O2、HO8910无细胞周期阻滞,各期细胞分别较对照组均匀;枸杞多糖组:枸杞多糖(500,1000,2000)mg/L作用下,L-O2生长抑制率分别为28%,31%,20%;SK-OV3为-1%,40%,35%,HO8910为13%,48%,41%;不同浓度LBP对L-O2及HO8910均有诱导凋亡作用,凋亡细胞数以1000mg/L为最大;1000mg/L组L-O2、HO8910细胞周期均阻滞于S期,S期细胞比例高于对照组。结论:枸杞原汁在体外对L-O2、SKOV3、HO8910有促进生长作用,且对HO8910的作用最大;对L-O2、HO8910无诱导细胞凋亡作用。枸杞多糖在体外对L-O2、SKOV3、HO8910都有抑制生长作用,且对HO8910作用最大;对L-O2、HO8910有诱导细胞凋亡作用,以浓度1000mg/L为最大,并未表现出剂量依赖效应。枸杞多糖诱导细胞发生S期阻滞,并且诱导S期细胞发生凋亡是其体外抑制细胞生长的可能机制之一。