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双语推荐:MDA

目的探索Erbin表达缺失导致Her2阳性的人乳腺癌细胞MDA-453对曲妥珠单抗敏感性的影响。方法设计、构建含人Erbin基因特异性的短发夹RNA(shRNA)及对照shRNA的干扰载体,转染MDA-453人乳腺癌细胞。经G418加压筛选,获得稳定敲低Erbin的MDA-453细胞(MDA-453-Erbin sh)和稳定表达对照shRNA的MDA-453细胞(MDA-453-NC),以后者作为对照细胞。应用Western印迹法检测MDA-453-NC和MDA-453-Erbin sh细胞中Erbin表达水平。分别通过细胞增殖活性实验及细胞集落形成实验,观察敲低Erbin的MDA-453细胞对曲妥珠单抗敏感性的变化。通过免疫组化染色法,分析Erbin在人乳腺癌及正常乳腺组织中的表达。结果建立了稳定敲低Erbin的MDA-453细胞株,发现敲低Erbin表达可诱导MDA-453细胞对曲妥珠单抗产生抗性。与正常乳腺上皮组织相比,人乳腺癌组织标本中Erbin表达水平降低。结论 Erbin表达缺失可能影响乳腺癌对曲妥珠单抗治疗的敏感性。
Objective To explore the effect of Erbin deficiency in MDA-453 cells on trastuzumab(Herceptin) resist-ance .Methods The specific short hairpin RNA ( shRNA) targeting Erbin was designed and cloned into plasmid pSuppres-sor, which was subsequently transfected into MDA-453 human breast cancer cells .After being selected by G418, MDA-453 cells stably expressing Erbin shRNA were obtained and nominated as MDA-453-Erbin sh.The MDA-453 cells express-ing control shRNA ( MDA-453-NC) were used as control cells .The expression of Erbin at the protein level in MDA-453-NC and MDA-453-Erbin sh cells was analyzed by Western blotting .Cell proliferation and colony formation assays were em-ployed to investigate the effect of Erbin knockdown on the sensitivity of MDA -453 cells to trastuzumab in vitro.The levels of Erbin expression in human breast cancer tissue and normal breast tissue samples were evaluated by immunohistochemistry . Results MDA-453 cells, in which Erbin expression was stably knocked-dow

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观察miR-374过表达对人乳腺癌MDA-MB-231细胞docetaxel(多西他赛)耐药性的影响。方法:qPCR检测miR-374过表达细胞MDA-MB-231-miR-374和对照细胞MDA-MB-231-Cherry中miR-374的相对含量;采用不同浓度的多西他赛处理细胞7 2小时后,MTT检测细胞的活性。在终浓度为3.2 nmol/L的多西他赛处理下,用平板克隆实验检测MDA-MB-231-Cherry和MDA-MB-231-miR-374细胞的增殖能力。流式细胞术检测细胞周期和凋亡。结果:与MDA-MB-231-Cherry细胞相比,miR-374过表达细胞MDA-MB-231-miR-374中miR-374的相对表达量明显增高;MDA-MB-231-miR-374细胞的耐药性和克隆形成能力明显增强(P0.05)。细胞凋亡率明显降低,G0/G1期细胞减少,S期细胞增加,G2/M期细胞增加。结论:miR-374过表达可明显增强乳腺癌细胞株MDA-MB-231对多西他赛的耐药性。
Objective:To investigate the effects of miR - 374 overexPression on docetaxel drug resistance of breast cancer cell line MDA - MB - 231. Methods:The relative exPressions of miR - 374 in MDA - MB - 231 - Cherry and MDA - MB - 231 - miR - 374 cell lines were identified by qPCR. The cells were Planted into 96 - well Plates and treated with different concentration of docetaxel,seventy - two hours later,cell viability was detected using MTT as-say. MDA - MB - 231 - Cherry and MDA - MB - 231 - miR - 374 cells were treated with docetaxel at a final concen-tration of 3. 2 nmol/ L,and colony - forming assay was used to detect the cell Proliferation activity. The cell aPoPtosis rate and cell cycle were detected by flow cytometry. Results:The relative exPression of miR - 374 in MDA - MB -231 - miR - 374 was significantly higher than that in MDA - MB - 231 - Cherry cells. ComPared with control cells, the Proliferation and colony - forming abilities of MDA - MB - 231 - miR - 374 cells imProves sign

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目的探讨mTOR在乳腺癌中的表达及其抑制剂CCI-779对乳腺癌细胞MDA-MB-231增殖及凋亡的影响。方法采用免疫组化SP法检测mTOR蛋白在乳腺癌组织和乳腺癌细胞MDA-MB-231中的表达;MTT法检测mTOR抑制剂CCI-779对MDA-MB-231细胞增殖的影响;应用AnnexinV-FITC/PI法检测CCI-779对MDA-MB-231细胞凋亡的影响。结果 mTOR蛋白在71例乳腺癌组织中的阳性率为54.9%,明显高于32例癌旁组织(阳性率为21.9%);MDA-MB-231细胞中亦存在mTOR蛋白的表达;mTOR抑制剂CCI-779对MDA-MB-231细胞的增殖具有显著抑制作用,呈浓度和时间依赖性;但CCI-779并不能诱导MDA-MB-231细胞发生凋亡。结论 mTOR与乳腺癌关系密切,其抑制剂CCI-779具有较强的抗MDA-MB-231细胞活性,有望成为乳腺癌治疗的前景药物。
Purpose To investigate the expression of mTOR in breast cancer, and to observe the effect of CCI-779 on proliferation and apoptosis of MDA-MB-231 cell. Methods Immunohistochemical staining was used to detect the expression of mTOR protein in breast cancer tissue and MDA-MB-231 cell. MTT method was used to show effect of CCI-779 on proliferation of MDA-MB-231 cell. Annex-inV-FITC/PI method was used to show effect of CCI-779 on apoptosis of MDA-MB-231 cell. Results 54.9% in 71 cases of breast cancer tissue could express mTOR protein, the expression was significantly higher than in 32 cases of normal tissue (21.9%), mTOR protein was also detected in MDA-MB-231 cell, CCI-779 could inhibit the proliferation of MDA-MB-231 cell, and show a dose-and time-dependent, but CCI-779 could not induce apoptosis of MDA-MB-231 with AnnexinV-FITC/PI assay. Conclusion mTOR is closely related to the formation of breast cancer, CCI-779 has strong activity against MDA-MB-231 cell, it has prospect f

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目的探讨木犀草素对乳腺癌细胞MDA-MB-231中SDF-1α/CXCR4信号通路抑制作用。方法采用不同浓度的木犀草素处理乳腺癌细胞MDA-MB-231,观察乳腺癌细胞MDA-MB-231的细胞增殖、趋化运动及CXCR4蛋白表达。结果木犀草素明显抑制乳腺癌细胞MDA-MB-231增殖,明显抑制乳腺癌细胞MDA-MB-231 CXCR4蛋白表达,并明显抑制SDF-1α/CXCR4对乳腺癌细胞MDA-MB-231的激活。结论木犀草素可抑制乳腺癌细胞MDA-MB-231增殖及SDF-1α/CXCR4介导的乳腺癌细胞的信号激活作用,在预防乳腺癌复发及转移中可能有重要的作用。
Objective To study the inhibition Effect of luteolin on SDF-1α/ CXCR4 signal pathway in breast cancer cells MDA-MB-231. Methods Different concentrations of luteolin were used to treat breast cancer cells MDA-MB-231,the cell enhancement,chemotactic migration and expression of CXCR4 were observed in breast cancer cells MDA-MB-231. Results Luteolin inhibited significantly the cell proliferation,the expression of CXCR4 and SDF-1α/ CXCR4 activation in the breast cancer cells of breast cancer cells MDA-MB-231. Conclusion Luteolin can inhibit the cell proliferation and SDF-1α/ CXCR4 signal activation of breast cancer cells MDA-MB-231,and may be important in the prevention of recurrence and metastasis of breast cancer.

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探讨小檗碱对人乳腺癌细胞MDA-MB-231体外生长的影响及其与PPARγ受体的关系。方法:采用噻唑蓝(MTT)法检测小檗碱对MDA-MB-231细胞的生长抑制效应;TUNEL法检测细胞凋亡;联合PPARγ拮抗剂GW 9662,分析小檗碱对MDA-MB-231细胞增殖的影响与PPARγ受体的关系。结果:小檗碱呈量-效和时-效关系抑制MDA-MB-231细胞生长,24 h的半数抑制浓度(IC50)为0.21μmol/L;小檗碱诱导MDA-MB-231细胞凋亡作用随药物浓度的增加而增强;PPARγ受体拮抗剂不能逆转小檗碱对细胞增殖的抑制作用。结论:小檗碱可明显抑制MDA-MB-231细胞生长并诱导其凋亡,但其作用不通过PPAR受体介导。
AIM: To investigate the anti-proliferation effect and its relationship to PPARγ/of berberine on human breast cancer cell line MDA-MB-231. METHODS: Cytostatic effect of berberine on MDA-MB-231 cells was measured by MTT. Apoptotic cells were determined by TUNEL. MDA-MB-231 cells were treated with berbcrine alone or in combination with PPARγ antagonist GW9662 to investigate the effect of berberine on cell proliferation and its relationship to PPARγ. RESULTS: MTT analysis detected that berberine inhibited growth of MDA-MB-231 cells in a dose and time-dependent manner with 0.21 pμmol/L IC50 value at 24 h post-treatment. Apparent apoptosis of MDA-MB-231 cells induced by berberine were also observed. PPARγ selective antagonist GW9662 could not reverse the inhibitory effect of berberine on proliferation of MDA-MB-231 cells. CONCLUSION: Berberine could induce MDA-MB-231 cells''apoptosis and inhibit the cells proliferation with independent of PPARγ activation.
目的:研究黑色瘤分化相关基因‐7(MDA‐7)/白细胞介素‐24(IL‐24)对食管癌细胞 Eca‐109与 TE‐1的增殖抑制作用和杀伤作用。方法应用RT‐PCR技术检测MDA‐7/IL‐24受体复合物在Eca‐109与 TE‐1细胞的表达,构建MDA‐7/IL‐24基因的重组腺病毒载体,将携带人MDA‐7/IL‐24基因的腺病毒Ad‐mda‐7分别感染食管癌细胞Eca‐109与TE‐1,通过Western‐blot检测MDA‐7基因的表达,通过CCK‐8检测该基因对食管癌细胞的增殖抑制作用,碘化丙啶(PI)染色后流式细胞仪检测MDA‐7对食管癌细胞周期的影响,Hoechst/PI双染色后流式细胞仪观察MDA‐7对食管癌细胞的诱导凋亡作用。结果 Eca‐109与 TE‐1均有表达MDA‐7/IL‐24受体复合物IL‐22R1/IL‐20R2;成功构建包装重组腺病毒,并经 Western‐blot验证其介导了外源基因 MDA‐7/IL‐24在Eca‐109与TE‐1细胞中的高效表达;CCK‐8实验结果表明,MDA‐7/IL‐24能显著抑制Eca‐109与 TE‐1细胞的增殖,且随着感染时间的延长及感染剂量的增加而增强抑制作用;细胞周期结果提示,MDA‐7/IL‐24使大量Eca‐109与TE‐1细胞被阻滞在G1~G0期;Hoechst/PI双染色结果提示,MDA‐7/IL‐24能明显促进Eca‐109与TE‐1细胞
Objective To study the effects of melanoma differentiation associated gene‐7/interleu‐kin 24 (MDA‐7/IL‐24) induction of grow th arrests and apoptosis on human esophageal cancer cell lines , Eca‐109 and TE‐1 . Methods The mRNA expressions of MDA‐7/IL‐24 receptor complexes in Eca‐109 and TE‐1 were confirmed using RT‐PCR . The MDA‐7/IL‐24 gene was transfected into Eca‐109 and TE‐1 with adenovirus vector . Protein expression was confirmed using Western‐blot . CCK‐8 assay and flow cytometry were used to analysis tumor cell proliferation and cell cycle separately . Flow cytometry assay after Hoechst and PI staining was performed to analysis the apoptosis . Results MDA‐7/IL‐24 receptor complexes IL‐22R1/IL‐20R2 was expressed in both Eca‐109 and TE‐1 . The protein product of MDA‐7/IL‐24 was detected in Eca‐109 and TE‐1 . MDA‐7/IL‐24 effectively inhibited the growth and proliferation of Eca‐109 and TE‐1 with the extension of time or the increase of MOI .

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目的探讨荜茇明碱(PL)对人乳腺癌MDA-MB-231细胞增殖、凋亡的影响及作用机制。方法体外培养人乳腺癌MDA-MB-231细胞;采用活细胞计数试剂盒(CCK-8)法检测不同浓度的PL对MDA-MB-231细胞增殖的影响;流式细胞术检测PL对细胞凋亡的影响;蛋白免疫印迹(Western blot)法检测PL对MDA-MB-231细胞Bcl-2和Bax蛋白表达水平的影响。结果PL抑制MDA-MB-231细胞增殖,并呈现出浓度、时间依赖性。PL诱导MDA-MB-231细胞凋亡,而乙酰-L-半胱氨酸则抑制了PL诱导的细胞凋亡。Western blot结果提示随着PL浓度的增加,Bax的表达逐渐增加,而Bcl-2的表达逐渐减少。结论 PL对人乳腺癌MDA-MB-231细胞有明显的生长抑制和诱导凋亡作用,其机制可能与Bcl-2蛋白表达的减少和Bax蛋白表达增加有关。
Objective The aim of the study was to investigate the effect of piplartine on the proliferation and apoptosis in human breast cancer MDA‐MB‐231 cells line and the mechanism involved .Methods Human breast cancer MDA‐MB‐231 cells line was cultured in vitro .The inhibitory effect of piplartine on the proliferation of MDA‐MB‐231 cells was measured by CCK‐8 assay after treatment with piplartine at different concentrations .The apoptosis rates were measured by flow cytometry .Western blot was used to explore the effect of piplartine on MDA‐MB‐231 cells Bcl‐2 and Bax protein expression .Results The CCK‐8 assay showed that piplartine had an inhibiting effect on the proliferation of MDA‐MB‐231 cells in a concentration and time dependent manner .Piplar‐tine induced apoptosis of MDA‐MB‐231 cells obviously .The antioxidant N‐acetyl‐L‐cystein inhibited the apoptosis of cells .By Western blot analysis ,we found the expression of Bax was up‐regulated whereas that of Bcl

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目的观察胰岛素样生长因子ⅡmRNA结合蛋白1(IMP1)的表达对人乳腺癌细胞增殖能力的影响。方法取对数生长期的人乳腺癌细胞株MDA231-IMP1-GFP和MDA231-GFP细胞,用10%胎牛血清DMEM培养液制成相同浓度的细胞悬液,加入培养板中分别培养24、48、72 h后,采用细胞计数板计数法及MTT检测法进行计数及比较。结果 IMP1的表达对细胞形态没有影响。在不同时间点,细胞计数板计数法及MTT法均显示,MDA231-IMP1-GFP细胞的增殖率低于MDA231-GFP(P均0.01)。结论 IMP1的表达对人乳腺癌细胞MDA231的增殖具有抑制作用。
Objective To investigate the effect of IMP1 on the proliferation of breast cancer cells.Methods Equal amounts of MDA231-IMP1-GFP cells and MDA231-GFP cells were cultured in DMEM medi-um containing 1 0% fetal bovine serum. Cell number was counted in 24,48,and 72 h with cell counting and MTT methods. The data was statistically analyzed. Results IMP1 had no impact on cellular morphology. In different time point,MDA231-IMP1-GFP cells proliferated more slowly than MDA231-GFP cells by cell count-ing and MTT methods (P<0.01 ). Conclusion IMP1 expression might inhibit the growth of human MDA231 breast cancer cells.

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目的 探讨断指再植患者术后血清丙二醛(malondialdehyde,MDA)含量及超氧化物歧化酶(superoxide dismutase,SOD)活性变化特点.方法 对40例患者分别于手术后1、24、48、72 h,第7、14 d检测血清MDA含量和SOD活性,另外取30例健康成年人检测血清MDA含量和SOD活性作为对照组进行对比分析.结果 断指再植患者术后1h至7d血清MDA含量逐渐升高,血清SOD活性明显降低,与对照组比较差异有统计学意义(P<0.05),术后14 d血清中MDA及SOD基本达到对照组水平(P>0.05).结论 术后检测MDA含量及SOD活性的变化可以指导临床用药,有效地防治血管危象的发生.
Objective To investigate the characteristic changes of serum malondialdehyde (MDA) and supemxide dismutase (SOD) levels in patients who had finger replantation.Methods Blood was drawn from 40 patients at 1,24,48,72 hours and 7,14 days after finger replantation to test the SOD activity and MDA content in the serum.Serum samples were,also collected from 30 healthy adults and analyzed to serve as control.Results Serum SOD activity was significantly reduced,while the serum MDA content increased gradually from 1 hour to 7 days after the operation.There were significant differences when compared to levels in the healthy control (P < 0.05).Serum SOD activity and MDA content basically reached the normal level 14 days later(P > 0.05).Conclusion Detection of serum SOD activity and MDA content after finger replantation can guide medication and prevent probability vascular crisis.

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背景与目的:统计表明90%以上肿瘤患者的死亡与肿瘤耐药相关,而在乳腺癌中常见PI3K/Akt/mTOR信号通路的异常激活,以此通路为靶点的药物已成为乳腺癌治疗的研究热点。本研究主要分析C族趋化因子配基1(C chemokine ligand 1,XCL1)对乳腺癌耐药细胞增殖的影响及其产生机制。方法:建立吉西他滨耐药性人乳腺癌细胞系MDA-MB-231/Gem。采用CCK8检测MDA-MB-231和MDA-MB-231/Gem的增殖能力,RT-PCR、ELISA检测2株细胞株XCL1表达差异,Western blot检测mTOR的表达。结果:与MDA-MB-231相比,MDA-MB-231/Gem的增殖能力增强,XCL1在耐药细胞株表达增强。mTOR在耐药细胞株表达水平及磷酸化水平增强。在MDA-MB-231中加入外源性XCL124 h后,细胞增殖能力增强。而在MDA-MB-231/Gem中加入抗XCL1抗体后,细胞增殖能力降低。mTOR抑制剂处理MDA-MB-231/Gem后,细胞增殖能力降低,XCL1产生减少。结论:趋化因子XCL1的分泌可促进乳腺癌耐药细胞的增殖并由mTOR信号通路介导产生。
Background and purpose: More than 90% of cancer patients are incurable because of drug resistance. Activation of PI3K/Akt/mTOR signaling pathway in breast cancer, as a target for chemotherapy drugs has become a hot topic of breast cancer treatment. This study aimed to investigate the effect and mechanism of XCL1 on the proliferation of drug-resistant breast cancer cell, whether is related with the mTOR signaling pathway. Methods:Established gemcitabine-resistant breast cancer cell lines (MDA-MB-231/Gem). CCK8 to detect the proliferation of MDA-MB-231 and MDA-MB-231/Gem, RT-PCR and ELISA to determine the XCL1 expression level of the two cell lines, Western blot to detect the expression of mTOR. Results:Compared with MDA-MB-231, MDA-MB-231/Gem showed an enhanced proliferative capacity. The expression of XCL1 was increased in the resistant cell lines. Both of protein level and phosphorylation level of mTOR increased in drug-resistant cell lines. The MDA-MB-231 added exogenous XC

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