雄激素受体在乳腺癌细胞中的表达及其对细胞增殖的影响

Objective To evaluate the expression of androgen receptor (AR) in the breast cancer cell lines and its effect on proliferation of breast cancer cells. Methods The estrogen receptor (ER) -positive MCF-7 and ER-negative MDA-MB-453 cells were involved in this study and cultured in vitro. The expression of AR was detected by using Western blotting. Cell proliferation was determined by methyl thiazol tetrazolium (MTT) assay after the treatment with different concentrations of dihydrotestosterone (DHT) ( 1 x 10 -7, 1 x 10- 8, 1 x 10 -9 mol/L) for 48, 96 and 144 h respectively. Cell cycle was analyzed by flow cytometry following culture for 72 h. Results DHT increased the AR expression in the two breast cancer cell lines. AR pathway could inhibit proliferation of MCF-7 and MDA-MB-453 cells. There was no significant difference in absorbance values among three treatment groups at different time points (P ＞ 0. 05). Cell cycle analysis revealed that the proportion of cells at G1 phase was increased, and that at S phase decreased. Conclusion AR pathway may inhibit proliferation of ER-negative MDA-MB-453 breast cells as well as ER-positive MCF-7 cells, by suppressing the process of G1 to S phase progression.     

雄激素受体在乳腺癌细胞中的表达及其对细胞增殖的影响

Objective To evaluate the expression of androgen receptor (AR) in the breast cancer cell lines and its effect on proliferation of breast cancer cells. Methods The estrogen receptor (ER) -positive MCF-7 and ER-negative MDA-MB-453 cells were involved in this study and cultured in vitro. The expression of AR was detected by using Western blotting. Cell proliferation was determined by methyl thiazol tetrazolium (MTT) assay after the treatment with different concentrations of dihydrotestosterone (DHT) ( 1 x 10 -7, 1 x 10- 8, 1 x 10 -9 mol/L) for 48, 96 and 144 h respectively. Cell cycle was analyzed by flow cytometry following culture for 72 h. Results DHT increased the AR expression in the two breast cancer cell lines. AR pathway could inhibit proliferation of MCF-7 and MDA-MB-453 cells. There was no significant difference in absorbance values among three treatment groups at different time points (P ＞ 0. 05). Cell cycle analysis revealed that the proportion of cells at G1 phase was increased, and that at S phase decreased. Conclusion AR pathway may inhibit proliferation of ER-negative MDA-MB-453 breast cells as well as ER-positive MCF-7 cells, by suppressing the process of G1 to S phase progression.     

慢病毒介导CCL5-siRNA对乳腺癌细胞生物学行为的影响

Objective To study the effect of lentivirus-mediated CCL5-RNAi on the biological behaviors of human breast cancer cells. Methods CCL5-specific siRNA gene was synthesized and cloned into the recombinant lentiviral vector, pGCSIL-GFP. Human high-metastatic breast cancer cells, MDA-MB-231, were infected by CCL5-siRNA recombinant lentivirus, which was set as KD group. Cells infected with CCL5-NC was as NC group, and cells cultured was as CON group. The expression of CCL5 mRNA and protein in MDA-MB-231 cells was detected by RT-PCR and western blot, respectively. Cell growth suppression and cell cycle was observed by MTT assay and fluorescence activated cell sorting (FACS). Colony formation and migration ability were determined by colony-rorming assay and Boyden chamber method. Results After infection of CCL5-siRNA recombinant lentivirus, the expression level of CCL5 mRNA and protein in MDA-MB-231 cells as well as the colony formation and migration ability decreased significantly, but cell's proliferation was not affected obviously. Compared with MDA-MB-231 (0.88± 0.15) and MDA-MB-231/CCL5-NC (1.00±0.07) cells, the expression of CCL5 mRNA in MDA-MB-231/ CCL5-siRNA decreased to 0.18±0.03, P<0.01. Compared with MDA-MB-231/CCL5-NC (1.82±0.18) cells, the expression of CCL5 protein in MDA-MB-231/CCL5-siRNA decreased to 0.33±0.13, P <0.01. Colony-forming assay and Boyden chamber method showed that the colony formation and migration ability of MDA-MB-231/CCL5-siRNA decreased markedly (P<0.05). The clone count in KD group was (0.33± 0.10), which was a significant decrease from (0.97±0.09) (NC group) and (1.04±0.07) (CON group), P<0.05. The number of cells that migrated through the chamber membrane of KD group (38± 15) was less than that of NC group (77±11, P <0.05) and CON group (69±9, P <0.05). However, MTT assay and FACS revealed that the proliferation of MDA-MB-231/CCL5-siRNA was not different from MDA-MB-231/CCL5-NC and MDA-MB-231 (P>0.05), the proliferation index (PI) of group KD, NC and CON were (0.48±0.02), (0.44±0.05) and (0.47±0.02) respectively. The difference was not statistically significant by multiple comparison (P>0.05). Conclusion CCL5-specific siRNA can specifically suppress the colony formation and migration of human high-matastatic breast cancer cells.     

慢病毒介导CCL5-siRNA对乳腺癌细胞生物学行为的影响

Objective To study the effect of lentivirus-mediated CCL5-RNAi on the biological behaviors of human breast cancer cells. Methods CCL5-specific siRNA gene was synthesized and cloned into the recombinant lentiviral vector, pGCSIL-GFP. Human high-metastatic breast cancer cells, MDA-MB-231, were infected by CCL5-siRNA recombinant lentivirus, which was set as KD group. Cells infected with CCL5-NC was as NC group, and cells cultured was as CON group. The expression of CCL5 mRNA and protein in MDA-MB-231 cells was detected by RT-PCR and western blot, respectively. Cell growth suppression and cell cycle was observed by MTT assay and fluorescence activated cell sorting (FACS). Colony formation and migration ability were determined by colony-rorming assay and Boyden chamber method. Results After infection of CCL5-siRNA recombinant lentivirus, the expression level of CCL5 mRNA and protein in MDA-MB-231 cells as well as the colony formation and migration ability decreased significantly, but cell's proliferation was not affected obviously. Compared with MDA-MB-231 (0.88± 0.15) and MDA-MB-231/CCL5-NC (1.00±0.07) cells, the expression of CCL5 mRNA in MDA-MB-231/ CCL5-siRNA decreased to 0.18±0.03, P<0.01. Compared with MDA-MB-231/CCL5-NC (1.82±0.18) cells, the expression of CCL5 protein in MDA-MB-231/CCL5-siRNA decreased to 0.33±0.13, P <0.01. Colony-forming assay and Boyden chamber method showed that the colony formation and migration ability of MDA-MB-231/CCL5-siRNA decreased markedly (P<0.05). The clone count in KD group was (0.33± 0.10), which was a significant decrease from (0.97±0.09) (NC group) and (1.04±0.07) (CON group), P<0.05. The number of cells that migrated through the chamber membrane of KD group (38± 15) was less than that of NC group (77±11, P <0.05) and CON group (69±9, P <0.05). However, MTT assay and FACS revealed that the proliferation of MDA-MB-231/CCL5-siRNA was not different from MDA-MB-231/CCL5-NC and MDA-MB-231 (P>0.05), the proliferation index (PI) of group KD, NC and CON were (0.48±0.02), (0.44±0.05) and (0.47±0.02) respectively. The difference was not statistically significant by multiple comparison (P>0.05). Conclusion CCL5-specific siRNA can specifically suppress the colony formation and migration of human high-matastatic breast cancer cells.     

慢病毒介导CCL5-siRNA对乳腺癌细胞生物学行为的影响

Objective To study the effect of lentivirus-mediated CCL5-RNAi on the biological behaviors of human breast cancer cells. Methods CCL5-specific siRNA gene was synthesized and cloned into the recombinant lentiviral vector, pGCSIL-GFP. Human high-metastatic breast cancer cells, MDA-MB-231, were infected by CCL5-siRNA recombinant lentivirus, which was set as KD group. Cells infected with CCL5-NC was as NC group, and cells cultured was as CON group. The expression of CCL5 mRNA and protein in MDA-MB-231 cells was detected by RT-PCR and western blot, respectively. Cell growth suppression and cell cycle was observed by MTT assay and fluorescence activated cell sorting (FACS). Colony formation and migration ability were determined by colony-rorming assay and Boyden chamber method. Results After infection of CCL5-siRNA recombinant lentivirus, the expression level of CCL5 mRNA and protein in MDA-MB-231 cells as well as the colony formation and migration ability decreased significantly, but cell's proliferation was not affected obviously. Compared with MDA-MB-231 (0.88± 0.15) and MDA-MB-231/CCL5-NC (1.00±0.07) cells, the expression of CCL5 mRNA in MDA-MB-231/ CCL5-siRNA decreased to 0.18±0.03, P<0.01. Compared with MDA-MB-231/CCL5-NC (1.82±0.18) cells, the expression of CCL5 protein in MDA-MB-231/CCL5-siRNA decreased to 0.33±0.13, P <0.01. Colony-forming assay and Boyden chamber method showed that the colony formation and migration ability of MDA-MB-231/CCL5-siRNA decreased markedly (P<0.05). The clone count in KD group was (0.33± 0.10), which was a significant decrease from (0.97±0.09) (NC group) and (1.04±0.07) (CON group), P<0.05. The number of cells that migrated through the chamber membrane of KD group (38± 15) was less than that of NC group (77±11, P <0.05) and CON group (69±9, P <0.05). However, MTT assay and FACS revealed that the proliferation of MDA-MB-231/CCL5-siRNA was not different from MDA-MB-231/CCL5-NC and MDA-MB-231 (P>0.05), the proliferation index (PI) of group KD, NC and CON were (0.48±0.02), (0.44±0.05) and (0.47±0.02) respectively. The difference was not statistically significant by multiple comparison (P>0.05). Conclusion CCL5-specific siRNA can specifically suppress the colony formation and migration of human high-matastatic breast cancer cells.     

乳腺癌干细胞放疗反应性和耐受机制的研究

Objective To discuss the response of breast cancer stem cells to radiation and its resistant mechanism. Methods Single breast cancer stem cells were isolated from the human breast adenocarcinoma cell line, MCF-7, and suspension-cultured into mammary cell microspheres in vitro. The radiosensitivity of these breast cancer stem cells were evaluated using a colony formation assay. Real-time polymerase chain reaction (PCR) was used to detect the expression levels of the following genes before and after radiation in the breast cancer stem cells, along with non-stem cells of the breast cancer cell line: ATM, p53, Her-2, Ku70/Ku80 and Survivin. Results The average survival fraction (SF2) of the suspensioncultured MCF-7 cells after 2 Gy of radiation was 0. 49, while the average SF2 of MCF-7 cells cultured as a monolayer was 0. 27 (P<0.01). Compared to the MCF-7 cells grown in a monolayer, the suspension-cultured MCF-7 cells had higher expression levels of ATM, p53, Her-2, Ku70/Ku80 and Survivin; The expression of ATM, p53, Her-2, Ku70/Ku80 and Survivin was 5. 29±1. 36,1. 37±0. 73,2.10±0. 57,4. 69±1. 45,and 1. 80±1.29 fold, respectively. Conclusion Breast cancer stem cells have stronger anti-radiation capabilities than breast cancer non-stem cells. The stronger DNA repair capacity is an important resistant mechanism about radiotherapy of breast cancer stem cells.     

乳腺癌干细胞放疗反应性和耐受机制的研究

Objective To discuss the response of breast cancer stem cells to radiation and its resistant mechanism. Methods Single breast cancer stem cells were isolated from the human breast adenocarcinoma cell line, MCF-7, and suspension-cultured into mammary cell microspheres in vitro. The radiosensitivity of these breast cancer stem cells were evaluated using a colony formation assay. Real-time polymerase chain reaction (PCR) was used to detect the expression levels of the following genes before and after radiation in the breast cancer stem cells, along with non-stem cells of the breast cancer cell line: ATM, p53, Her-2, Ku70/Ku80 and Survivin. Results The average survival fraction (SF2) of the suspensioncultured MCF-7 cells after 2 Gy of radiation was 0. 49, while the average SF2 of MCF-7 cells cultured as a monolayer was 0. 27 (P<0.01). Compared to the MCF-7 cells grown in a monolayer, the suspension-cultured MCF-7 cells had higher expression levels of ATM, p53, Her-2, Ku70/Ku80 and Survivin; The expression of ATM, p53, Her-2, Ku70/Ku80 and Survivin was 5. 29±1. 36,1. 37±0. 73,2.10±0. 57,4. 69±1. 45,and 1. 80±1.29 fold, respectively. Conclusion Breast cancer stem cells have stronger anti-radiation capabilities than breast cancer non-stem cells. The stronger DNA repair capacity is an important resistant mechanism about radiotherapy of breast cancer stem cells.     

雄激素对MCF-7乳腺癌细胞株增殖凋亡的影响

目的 观察睾丸酮对MCF-7乳腺癌细胞株增殖、凋亡的影响,并探讨其机制.方法 将1×10~(-5)、1×10~(-7)、1×10~(-9)、1×10~(-11) mol/L的睾丸酮分别作用于乳腺癌MCF-7细胞24、48、72 h,噻唑蓝(MTT)比色法检测细胞生长,流式细胞术检测不同浓度睾丸酮作用48 h时MCF-7细胞的周期分布和凋亡以及该细胞株中细胞周期素D1蛋白和雄激素受体的表达.结果 高浓度睾丸酮抑制MCF-7乳腺癌细胞株的增殖,1×10~(-5) mol/L睾丸酮作用48 h时,细胞生长抑制率为22.21%,细胞凋亡率为(58.60±5.41)%,但可使细胞周期由G_1 期进入S期,并可使细胞周期素D1蛋白表达量增加,雄激素受体蛋白表达量下降.低浓度睾丸酮(1×10~(-9) mol/L)作用后细胞周期素D1蛋白表达量无明显变化,雄激素受体蛋白表达量升高,在短时间内(24 h)可促进MCF-7细胞增殖.结论 高浓度睾丸酮在体外可使MCF-7乳腺癌细胞株细胞周期素D1蛋白表达增加,使细胞周期由G_1进入S期,而同时促使细胞凋亡,表现出抗肿瘤作用.低浓度睾丸酮有短暂的促进MCF-7乳腺癌细胞增殖的作用.     

RNA干扰下调midkine基因表达对人乳腺癌细胞粘附和侵袭力的影响

目的 探讨中期因子(midkine,MK)基因siRNA对乳腺癌细胞生物学行为的影响.方法 培养人乳腺癌Bcap-37、LCCI、MCF-7、MDA-MB-231、MDA-MB-435、MDA-MB-468及ZR75-1细胞株,以荧光实时定量PCR方法检测MK基因mRNA表达;筛选出MK表达最高者.采用MK siRNA...     

反义RNA抑制Ezrin表达对乳腺癌细胞侵袭能力的影响

目的 观察特异性阻断Ezrin的表达对人乳腺癌细胞MDA-MB-231和MCF-7的增殖和侵袭能力的影响.方法 将anti-pCR3.1-Ezrin质粒经脂质体介导,转染人人乳腺癌细胞MDA-MB-231 6、12和24 h,应用Western blot和逆转录-聚合酶链反应(RT-PCR)方法检测Ezrin的表达变化情况;转染质粒24h后,噻唑蓝(MTT)比色法检测抑制Ezrin对MDA-MB-231和MCF-7细胞体外增殖能力的影响,Boyden小室法检测抑制Ezrin对MDA-MB-231和MCF-7细胞体外侵袭能力的影响.结果 转染anti-pCR3.1-Ezrin后,对MDA-MB-231细胞中的Ezrin表达抑制在24 h时达高峰.MTT法比色实验结果显示,MDA-MB-231和MCF-7细胞中转染anti-pCR3.1-Ezrin组、转染空质粒组和对照组的A值分别为0.410±0.018、0.765±0.058、0.795±0.061和0.480±0.021、0.632±0.052、0.648±0.059.转染anti-pCR3.1-Ezrin组细胞的增殖受到明显抑制,抑制率分别为(47.9±3.1)%和(32.0±2.8)%(P<0.05).Boyden小室法检测结果显示,MDA-MB-231和MCF-7细胞中转染anti-pCR3.1-Ezrin组细胞的侵袭能力分别为对照组的(50.5±3.2)%和(74.8±4.6)%(P<0.05).结论 Ezrin在乳腺癌的生长和侵袭过程中发挥重要作用.     

长链非编码RNA RP1-85F18.6在乳腺癌细胞中的表达及其对增殖和细胞周期的影响

背景与目的:近年来,大量研究表明长链非编码RNA(lncRNA)在肿瘤发生、发展中起着重要作用。lncRNA RP1-85F18.6是新近发现的非编码RNA,其在结肠癌组织和细胞系中高表达,并可促进肿瘤细胞增殖和侵袭,抑制凋亡及调控细胞周期。然而,目前尚无lncRNA RP1-85F18.6在乳腺癌中的研究报道,因此,本研究初步探讨lncRNA RP1-85F18.6在乳腺癌细胞中的表达及其对增殖和细胞周期的影响。方法:qRT-PCR法检测lncRNA RP1-85F18.6在乳腺癌细胞系MDA-MB-231、MBA-MD-468、MCF-7 及正常乳腺细胞系MCF-10A中的表达。将MDA-MB-231细胞分别转染RP1-85F18.6沉默序列(沉默组)与阴性对照序列(阴性对照组),将无处理的MDA-MB-231细胞作为空白对照组,在各组细胞中采用MTT法测定增殖能力,PI染色流式细胞仪检测法测定细胞周期,Western blot法测定Ki-67、增殖细胞核抗原(PCNA)、cyclin A1和p21~(C1P1)蛋白的表达。结果:乳腺癌细胞系MDA-MB-231、MBA-MD-468及MCF-7中lncRNA RP1-85F18.6相对表达量均高于正常乳腺上皮细胞系MCF-10A(均P0.05)。沉默组在转染后24、48、72、96 h的OD_(490) _(nm)值均明显低于空白对照组(均P0.05)。与空白对照组比较,沉默组的G_1/G_0期细胞比例无明显变化(P0.05),但S期细胞比例明显升高、G_2/M期细胞比例明显降低(均P0.05);沉默组Ki67﹑PCNA及cyclin A1蛋白表达量明显下调,而p21~(C1P1)蛋白表达量明显上调(均P0.05)。阴性对照组与空白对照组间以上指标差异均无统计学意义(均P0.05)。结论:lncRNA RP1-85F18.6在乳腺癌细胞系中高表达,其可能通过调节增殖相关蛋白及细胞周期蛋白的表达而参与乳腺癌的发生与发展,对lncRNA RP1-85F18.6及其相关靶基因的干预可能为乳腺癌的治疗提供新的途径。     

尿多酸肽对乳腺癌细胞凋亡的影响

目的研究肿瘤细胞分化诱导剂尿多酸肽（CDA—Ⅱ）对乳腺癌细胞凋亡的影响。方法将CDA—Ⅱ与不同生物学特性的乳腺癌细胞株MCF-7和MDA-MB-231进行体外培养，同时以维甲酸为阳性对照，观察CDA—Ⅱ对乳腺癌细胞生长曲线、细胞凋亡及形态学等方面的影响。结果CDA—Ⅱ可减缓两株乳腺癌细胞的生长和增殖能力，诱导乳腺癌细胞凋亡。结论CDA—Ⅱ可抑制MCF-7和MDA-MB-231两株乳腺癌细胞的生长和增殖能力，诱导乳腺癌细胞凋亡．本研究为CDA-Ⅱ治疗乳腺痛提供了实验依据。     

1,25二羟维生素D3与5-氟尿嘧啶对乳腺癌细胞生长及凋亡的影响

目的研究1，25二羟维生素D3[1，25(OH)2D3]与5-氟尿嘧啶(5-Fu)对人乳腺癌细胞株MCF-7生长及凋亡的影响。方法采用噻唑蓝(MTT)比色法分析细胞生长抑制作用，流式细胞术测定细胞周期和凋亡率，免疫组织化学法检测bcl-2蛋白表达。结果1，25(OH)2D3与5-Fu均可抑制MCF-7细胞生长、1，25(OH)2D3阻滞细胞周期于G0／G1期，5-Fu阻滞细胞周期于S期，并可诱导细胞凋亡；当两药联合应用时，上述作用得到显著加强，凋亡率明显上升。两药均可下调bcl-2蛋白表达，当两药联合应用时，bcl-2蛋白几乎不表达。结论1，25(OH)2D3与5-Fu联合应用对乳腺癌细胞具有协同抑制生长和诱导凋亡作用。     

人平衡型核苷载体在乳腺癌细胞中的表达情况及其对5-FU药效的影响

目的研究乳腺癌细胞株MDA-MB-231、MDA-MB-468、SK-BR-3、MCF-7中人平衡型核苷载体（hENTS）的表达及其对5氟尿嘧啶（5-Fu）细胞毒性的影响。方法MDA-MB-231、MDA—MB-468、SK-BR-3、MCF-7细胞常规培养于含10％小牛血清的高糖DMEM培养液中。逆转录．聚合酶链反应（RT-PCR）检测4种细胞株中hENTlmRNA及hENT2mRNA的表达。每种细胞分别在含有一定浓度序列（1．28×10^4ng／L～2．00×10^8ng／L）5-FU的培养液中培养48h。MTT法检测4种细胞株增殖,并计算其5-FU的半数抑制浓度（IC50）。结果①bENT1及hENT2mRNA在MDA-MB-231、MDA-MB-468、SK-BR-3细胞中的表达均较其在MCF-7细胞中（P伊〈0．05）,但其表达在MDA-MB-231、MDA-MB-468、SK-BR-3细胞中差异无统计学意义（P〉0．05）。hENT2mRNA表达在4种细胞中均较hENT1 mRNA表达低,差异有统计学意义（P〈0．05）。②MTT结果显示,5-FU的IC50在MDA-MB-231、MDA-MB-468、SK-BR-3细胞株中均较在MCF-7细胞株中低（P〈0．05）,在MDA-MB-231、MDA-MB-468、SK-BR-3细胞株之间差异无统计学意义（P〉0．05）。③在5-FU的IC50 较低的乳腺癌细胞株（MDA-MB-231、MDA—MB-468、SK-BR-3）中高表达hENTs,而在5-Fu的Ic50较高的乳腺癌细胞株（MCF-7）中,低表达hENTs或无表达。结论在乳腺癌细胞株中,细胞膜上hENTs的表达情况能显著影响5-FU的作用效果,其结果提示,在临床上可能需要依据hENTs的表达情况来选择核苷类抗癌药物。     

核转录因子κB激活对雌激素受体阴性乳腺癌细胞增殖的影响

目的研究雌激素受体（ER）阴性乳腺癌细胞株中核转录因子κB的激活途径及其促进肿瘤细胞增殖的机制。方法以蛋白印迹法和流式细胞技术研究不同受体类型乳腺癌细胞株IκB激酶α表达、不同处理因素对雌激素受体阴性细胞株MDA-MB-435S细胞周期的影响,以及抑制核转录因子κB对细胞增殖的影响。结果雌激素受体阴性细胞株中的IκB激酶α表达高于受体阳性细胞株,而在MDA-MB-435S中促进细胞增殖因素的研究中,表皮生长因子作用最显著,它能提高细胞周期蛋白D1表达,较对照组增加83％,促细胞增殖指数由0．22提高至0．31（P〈0．01）,而应用蛋白激酶C抑制剂C06976抑制核转录因子κB激活,可显著抑制表皮生长因子的促细胞增殖作用。结论表皮生长因子的促雌激素受体阴性乳腺癌细胞增殖信号可通过激活核转录因子κB提高细胞周期蛋白D1表达,促进了肿瘤细胞增殖。核转录因子κB起了增殖信号递呈作用,针对核转录因子κB激活的治疗可提供乳腺癌全新的治疗靶点。     

熊果酸对MCF-7乳腺癌细胞生长的影响

目的 观察熊果酸对MCF-7乳腺癌细胞增殖、凋亡、细胞侵袭及裸鼠移植瘤生长的影响.方法 将1、10、100 μmol/L的熊果酸分别作用于乳腺癌MCF-7细胞12、24、48 h,噻唑蓝(MTT)比色法检测细胞活力变化及生长抑制率,流式细胞术及Transwell小室法检测熊果酸作用48h时MCF-7细胞周期、细胞凋亡率及细胞侵袭力.将乳腺癌MCF-7细胞接种于裸鼠,成瘤后分为生理盐水对照组、熊果酸低剂量组(每日1 mg/kg)、中剂量组(每日5 mg/kg)和高剂量组(每日25 mg/kg),检测5、10、15 d裸鼠移植瘤体积、肿瘤生长抑制率及15 d时肝肾功能、血常规变化.结果 随熊果酸浓度增加及作用时间延长,MCF-7细胞生长及凋亡发生受到显著影响,100 μmol/L熊果酸作用48 h时,细胞生长抑制率为46.0%,生长周期阻滞于G0/G1期,细胞凋亡率为(16.48±2.46)%,细胞侵袭力显著下降.熊果酸组裸鼠移植瘤体积显著小于对照组,15 d时熊果酸高剂量组肿瘤体积为(323.5±33.5)mm3生长抑制率为50.9%.各组肝肾功能和血常规无明显变化.结论 熊果酸可引起体外乳腺癌McF-7细胞增殖抑制、细胞凋亡率增加及细胞侵袭力下降,可显著抑制裸鼠乳腺癌移植瘤生长.