乳腺癌不同肺转移潜能细胞株蛋白组学比较及其差异蛋白调控的研究
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摘要
目的:以具有不同肺转移潜能的乳腺癌细胞为模型,研究乳腺癌转移分子机制,并筛选潜在的乳腺癌转移蛋白标志物。
方法:核型分析确定所建立的具有自发性肺高转移特性的人乳腺癌细胞株MDA-MB-231 HM来自亲代MDA-MB-231,并在体外通过transwell和体内比较原位瘤重量和小鼠肺转移灶数目分析两者转移能力强弱,进一步通过双向凝胶电泳技术作两种细胞的胞内蛋白组学比较,对差异蛋白作质谱鉴定,再挑选所鉴定到的蛋白作western blot和免疫组化作进一步深入验证。
结果:MDA-MB-231 HM的染色体均为“X”形状,不同于小鼠染色体的“V”形状,由此断定从小鼠肺部分离到的MDA-MB-231 HM为人类细胞,来自MDA-MB-231;体内和体外侵袭转移能力比较发现MDA-MB-231 HM转移能力高过亲代MDA-MB-231;蛋白组学比较并鉴定到14个差异蛋白,这些蛋白包括:Macrophage-capping protein(CapG)、Galectin-1、Chloride intracellular channelprotein 1、Endoplasmic reticulum protein ERp29 precursor、Transgelin-2、Peptidyl-prolyl cis-trans isomerase A(PPIase A)、Stathmin-1(STMN1)、Isoform 1 ofUridine-cytidine kinase 2(UCK2)、Rho GDP-dissociation inhibitor 2(ARHGDIB)、Isocitrate dehydrogenase[NADP]cytoplasmic(IDH1)、NDRG1 Protein NDRG1、Sperm protein associated with the nucleus on the X chromosome B/F、Neuron-specific calcium-binding hippocalcin、HSPA5 protein。其中Transgelin-2、HSPA5 protein在MDA-MB-231HM细胞中下调表达,Sperm protein associatedwith the nucleus on the X chromosome B/F、hippocalcin在MDA-MB-231HM中缺失,CapG、Galectin-1、Chloride intracellular channel protein 1、ERp29、PPIase A、STMN1、UCK2、Rho GDP-dissociation inhibitor 2、Isocitrate dehydrogenase[NADP]cytoplasmic(IDH1)、NDRG1均在MDA-MB-231HM细胞中上调表达,挑选其中的CapG、STMN1和transgelin-2作western blot分析进一步发现CapG、STMN1在MDA-MB-231HM细胞中上调表达,transgelin-2则下调表达。对transgelin-2作人乳腺癌肿瘤组织免疫组化发现transgelin-2表达与淋巴结转移阴性病例高相关(19/30),而与淋巴结转移阳性病例低相关(5/30)。这些实验数据为临床诊断乳腺癌转移提供了具有参考价值的蛋白标志物。
结论:以肺高转移细胞株MDA-MB-231HM为模型,可为研究乳腺癌转移的机制提供一个良好的平台,所筛选的14个蛋白不仅可揭示乳腺癌转移的分子机制,还可为临床诊断乳腺癌转移提供潜在的蛋白标志物。
目的:比较不同肺转移潜能的乳腺癌细胞株的分泌蛋白组,为临床诊断筛选分泌相关的乳腺癌转移蛋白标志物,并进一步研究差异分泌蛋白的调控因素。
方法:采用无血清培养基培养MDA-MB-231HM细胞和MDA-MB-231细胞24小时后,超滤法脱盐并浓缩细胞培养上清制备分泌蛋白质,采用双向凝胶电泳技术分离蛋白质,应用基质辅助激光解吸电离飞行时间质谱和生物信息学资源鉴定差异分泌的蛋白质。Weaern blot和RT-PCR进一步验证差异蛋白基质金属蛋白酶1(MMP1)的差异表达和分泌。体外构建靶向MMP1基因的shRNA质粒和阴性对照质粒,Lipofectamine2000介导转染到MDA-MB-231细胞中,Transwell实验检测细胞体外侵袭转移力,进一步验证MMP1转移方面的功能。为研究对MMP1分泌有调控的蛋白,对MMP1进行免疫共沉淀,质谱鉴定沉淀复合物成分,再用激光共聚焦和免疫共沉淀技术来研究复合物中热休克蛋白GRP75和MMP1的相互作用。为研究胞内对MMP1表达的影响,用CXCR4的特异性抑制剂AMD3100干扰T47D细胞、MDA-MB-231HM细胞和MDA-MB-231细胞来研究CXCR4对MMP1的调控。
结果:分泌蛋白组学比较得到22个差异蛋白,质谱鉴定到五种蛋白包括pro-MMP1、mature-MMP1、TIMP-2、TCTP和beta-2 microglobulin。其中MMP1和TCTP在MDA-MB-231HM细胞中上调分泌,TIMP-2和beta-2 microglobulin在MDA-MB-231HM细胞中下调分泌。Weaern blot和RT-PCR均证实MMP1在MDA-MB-231HM细胞中上调表达和分泌,且分泌层次的差异明显高过胞内表达的差异。Transwell显示RNA干扰MDA-MB-231细胞中的MMP1蛋白36小时后与转染空载质粒MDA-MB-231细胞相比,干扰组穿过基底膜的细胞数量明显减少。在MMP1免疫共沉淀复合物中鉴定到GRP75,用抗GRP75的抗体对GRP75进行免疫共沉淀,复合物中western blot检测到MMP1,激光共聚焦显示GRP75和MMP1存在共定位,但western blot显示GRP75在MDA-MB-231HM细胞和MDA-MB-231细胞内表达无差异。而使用AMD3100干扰的T47D细胞、MDA-MB-231HM细胞和MDA-MB-231细胞内,MMP1表达均下调。
结论:不同肺转移潜能的乳腺癌细胞株存在多种蛋白差异分泌。MMP1对乳腺癌细胞转移侵袭有促进作用,可能是潜在的乳腺癌转移标志物。MMP1在促进癌症转移的过程中,与表达差异相比,分泌差异可能起主要促进作用。GRP75和MMP1存在相互作用,但GRP75对MMP1的作用可能不是影响MDA-MB-231HM细胞和MDA-MB-231细胞差异分泌MMP1的原因,而在乳腺癌细胞中CXCR4可能对MMP1表达存在调控作用。
Objective:To use human breast cancer cell lines with differently spontaneous lung metastatic capability as suitable models for the study of the molecular mechanisms related to breast cancer metastasis and finding out protein markers with metastatic potential.
Methods:MDA-MB-231HM was identified as one kind of cell lines derived from parental MDA-MB-231 cells by analyzing the karyotype of the MDA-MB-231HM cells with Giemsa chromosome banding stain.Then metastatic potential of both cell lines was tested in vitro by transwell and in vivo by comparing the weight of orthotopic tumor and the number of metastasis.Using two-dimensional electrophoresis(2-DE),we performed a proteomic comparison of both cell lines. Subsequently differentially expressed protein spots were identified by mass spectrometry.Differential expression was confirmed by Western blotting analysis and immunohistochemistry.
Results:All the MDA-MB-231HM cells exhibited X shaped chromosomes, which is completely different fromⅤshaped chromosomes of mice.Metastatic potential of MDA-MB-231HM cells was found higher than that of MDA-MB-231cells both in vitro and in vivo.We finally identified 14 unique proteins by proteomic analysis including Macrophage-capping protein(CapG),Galectin-1, Chloride intracellular channel protein 1,Endoplasmic reticulum protein ERp29 precursor,Transgelin-2,Peptidyl-prolyl cis-trans isomerase A(PPIase A),Stathmin-1 (STMN1),Isoform 1 of Uridine-cytidine kinase 2(UCK2),Rho GDP-dissociation inhibitor 2(ARHGDIB),Isocitrate dehydrogenase[NADP]cytoplasmic(IDH1), NDRG1 Protein NDRG1,Sperm protein associated with the nucleus on the X chromosome B/F,Neuron-specific calcium-binding hippocalcin,HSPA5 protein. Transgelin-2 and HSPA5 protein were down-regulated in MDA-MB-231HM cells, whereas Sperm protein associated with the nucleus on the x chromosome B/F and hippocalcin were only detected in MDA-MB-231 cells.CapG,Galectin-1,Chloride intracellular channel protein 1,ERp29,PPIase A,STMN1,UCK2,Rho GDP-dissociation inhibitor 2,Isocitrate dehydrogenase[NADP]cytoplasmic(IDH1) and NDRG1 were up-regulated in MDA-MB-231HM cells.Change of CapG,STMN1 and transgelin-2 was confirmed by western blotting analysis.Immunohistochemical analysis showed transgelin-2 expression was higher correlation in lymph node-negative tissues(19/30) and lower correlation in lymph node-positive tissues (5/30).
Conclusions:MDA-MB-231HM,a human breast carcinoma cell line with high capability of spontaneous lung metastasis,was a good tool for the study of breast cancer metastasis.Fourteen unique proteins in our study can both reveal molecular mechanisms related to breast cancer metastasis and be used as biological markers with metastatic potential for clinical diagnosis in breast cancer metastasis.
Objective:To compare the secretome of both human breast cancer cell lines with differently spontaneous lung metastatic capability for finding out biological markers with metastatic potential for clinical diagnosis in breast cancer metastasis. Further more,to study the regulation of the protein differently secreted by MDA-MB-231HM cells and MDA-MB-231 cells.
Methods:MDA-MB-231HM cells and MDA-MB-231 cells were cultured in serum-free medium for 24 hours,and the culture supernant of cells was desalted and concentrated by ultrafiltration to prepare the total secreted proteins.Two-dimensional gel electrophoresis(2-DE) was used to separate the secreted proteins.The differently secreted protein spots gels were identified by desorption/ionization time-of-flight mass spectrometry(MALDI-TOF-MS) and bioinformatics.Western blot and RT-PCR were used to further confirm differential expression and secretion of matrix metalloproteinase 1(MMP1).The expression vector of MMP1 specific shRNA(short hairpin RNA) and negative shRNA in vitro were constructed and transfected into MDA-MB-231 cells by lipofectamine2000 for the study of the function of MMP1 related to metastasis.The potential of invasion in vitro was tested by Transwell experiment.When MMP1 was immunoprecipitated by anti-MMP1 antibody for the study of the secretory regulation of MMP1,components from immunoprecipitated complex was separated by SDS-polyaerylamide gel electrophoresis and then identified by mass spectrometry.Interaction of MMP1 and GRP75 from immunoprecipitated complex was studied by confocalmicroscopy and co-immunoprecipitation.CXCR4 antagonist AMD3100 was used to interfere T47D cells,MDA-MB-231HM cells and MDA-MB-231 cells to study whether CXCR4 can affect the expressive regulation of MMP1.
Results:The secretory protein profiles reveal 22 proteins differently secreted by MDA-MB-231HM cells and MDA-MB-231 cells,whereas only five protein spots were identified by MALDI-TOF-MS including pro-MMP1,mature-MMP1,TIMP-2, TCTP,beta-2 microglobulin.MMP1 and TCTP were up-regulated in MDA-MB-231HM cells,whereas TIMP-2 and beta-2 microglobulin were up-regulated in MDA-MB-231 cells.Up-regulated expression and secretion of MMP1 were confirmed by western blot and RT-PCR,which also revealed secretory difference of both cell lines was more significant than expressive difference of both cell lines.Transwell experiment revealed that the number of MDA-MB-231 cells into which were transfected by the vector of MMP1 specific shRNA for 36 hours to penetrate polycarbonates coated with Matrigel was significantly lower than that of MDA-MB-231 cells into which were transfected by the vector of MMP1 negative shRNA for 36 hours.GRP75 was identified in immunoprecipitated complex.When MMP1 was immunoprecipitated by anti-MMP1 antibody,MMP1 was identified by western blotting with anti-MMP1 antibody from immunoprecipitated complex. Co-localization of GRP75 and MMP1 was determined by confocalmicroscopy, whereas western blot revealed there was no differently expressive amount of GRP75 between MDA-MB-231 cells and MDA-MB-231HM cells.AMD3100 can down-regulated the expression of MMP1 in T47D cells,MDA-MB-231HM cells and MDA-MB-231 cells.
Conclusions:Many kinds of secretory proteins were differently secreted from both human breast cancer cell lines with differently spontaneous lung metastatic capability.MMP1 may contribute to breast cancer metastasis and be used as a potential protein marker related to breast cancer metastasis.Contrasted with differently internal expression of MMP1 between the interior of MDA-MB-231 cells and MDA-MB-231HM cells,differently secretion of MMP1 between MDA-MB-231 cells and MDA-MB-231HM cells may play a predominant role in enhancing metastatic potential.GRP75 can interact with MMP1,whereas this kind of interaction may not be the effect of different secretion of MMP1 between MDA-MB-231 cells and MDA-MB-231HM cells.CXCR4 may regulate the expression of MMP1 in breast cancer cells.
方法:核型分析确定所建立的具有自发性肺高转移特性的人乳腺癌细胞株MDA-MB-231 HM来自亲代MDA-MB-231,并在体外通过transwell和体内比较原位瘤重量和小鼠肺转移灶数目分析两者转移能力强弱,进一步通过双向凝胶电泳技术作两种细胞的胞内蛋白组学比较,对差异蛋白作质谱鉴定,再挑选所鉴定到的蛋白作western blot和免疫组化作进一步深入验证。
结果:MDA-MB-231 HM的染色体均为“X”形状,不同于小鼠染色体的“V”形状,由此断定从小鼠肺部分离到的MDA-MB-231 HM为人类细胞,来自MDA-MB-231;体内和体外侵袭转移能力比较发现MDA-MB-231 HM转移能力高过亲代MDA-MB-231;蛋白组学比较并鉴定到14个差异蛋白,这些蛋白包括:Macrophage-capping protein(CapG)、Galectin-1、Chloride intracellular channelprotein 1、Endoplasmic reticulum protein ERp29 precursor、Transgelin-2、Peptidyl-prolyl cis-trans isomerase A(PPIase A)、Stathmin-1(STMN1)、Isoform 1 ofUridine-cytidine kinase 2(UCK2)、Rho GDP-dissociation inhibitor 2(ARHGDIB)、Isocitrate dehydrogenase[NADP]cytoplasmic(IDH1)、NDRG1 Protein NDRG1、Sperm protein associated with the nucleus on the X chromosome B/F、Neuron-specific calcium-binding hippocalcin、HSPA5 protein。其中Transgelin-2、HSPA5 protein在MDA-MB-231HM细胞中下调表达,Sperm protein associatedwith the nucleus on the X chromosome B/F、hippocalcin在MDA-MB-231HM中缺失,CapG、Galectin-1、Chloride intracellular channel protein 1、ERp29、PPIase A、STMN1、UCK2、Rho GDP-dissociation inhibitor 2、Isocitrate dehydrogenase[NADP]cytoplasmic(IDH1)、NDRG1均在MDA-MB-231HM细胞中上调表达,挑选其中的CapG、STMN1和transgelin-2作western blot分析进一步发现CapG、STMN1在MDA-MB-231HM细胞中上调表达,transgelin-2则下调表达。对transgelin-2作人乳腺癌肿瘤组织免疫组化发现transgelin-2表达与淋巴结转移阴性病例高相关(19/30),而与淋巴结转移阳性病例低相关(5/30)。这些实验数据为临床诊断乳腺癌转移提供了具有参考价值的蛋白标志物。
结论:以肺高转移细胞株MDA-MB-231HM为模型,可为研究乳腺癌转移的机制提供一个良好的平台,所筛选的14个蛋白不仅可揭示乳腺癌转移的分子机制,还可为临床诊断乳腺癌转移提供潜在的蛋白标志物。
目的:比较不同肺转移潜能的乳腺癌细胞株的分泌蛋白组,为临床诊断筛选分泌相关的乳腺癌转移蛋白标志物,并进一步研究差异分泌蛋白的调控因素。
方法:采用无血清培养基培养MDA-MB-231HM细胞和MDA-MB-231细胞24小时后,超滤法脱盐并浓缩细胞培养上清制备分泌蛋白质,采用双向凝胶电泳技术分离蛋白质,应用基质辅助激光解吸电离飞行时间质谱和生物信息学资源鉴定差异分泌的蛋白质。Weaern blot和RT-PCR进一步验证差异蛋白基质金属蛋白酶1(MMP1)的差异表达和分泌。体外构建靶向MMP1基因的shRNA质粒和阴性对照质粒,Lipofectamine2000介导转染到MDA-MB-231细胞中,Transwell实验检测细胞体外侵袭转移力,进一步验证MMP1转移方面的功能。为研究对MMP1分泌有调控的蛋白,对MMP1进行免疫共沉淀,质谱鉴定沉淀复合物成分,再用激光共聚焦和免疫共沉淀技术来研究复合物中热休克蛋白GRP75和MMP1的相互作用。为研究胞内对MMP1表达的影响,用CXCR4的特异性抑制剂AMD3100干扰T47D细胞、MDA-MB-231HM细胞和MDA-MB-231细胞来研究CXCR4对MMP1的调控。
结果:分泌蛋白组学比较得到22个差异蛋白,质谱鉴定到五种蛋白包括pro-MMP1、mature-MMP1、TIMP-2、TCTP和beta-2 microglobulin。其中MMP1和TCTP在MDA-MB-231HM细胞中上调分泌,TIMP-2和beta-2 microglobulin在MDA-MB-231HM细胞中下调分泌。Weaern blot和RT-PCR均证实MMP1在MDA-MB-231HM细胞中上调表达和分泌,且分泌层次的差异明显高过胞内表达的差异。Transwell显示RNA干扰MDA-MB-231细胞中的MMP1蛋白36小时后与转染空载质粒MDA-MB-231细胞相比,干扰组穿过基底膜的细胞数量明显减少。在MMP1免疫共沉淀复合物中鉴定到GRP75,用抗GRP75的抗体对GRP75进行免疫共沉淀,复合物中western blot检测到MMP1,激光共聚焦显示GRP75和MMP1存在共定位,但western blot显示GRP75在MDA-MB-231HM细胞和MDA-MB-231细胞内表达无差异。而使用AMD3100干扰的T47D细胞、MDA-MB-231HM细胞和MDA-MB-231细胞内,MMP1表达均下调。
结论:不同肺转移潜能的乳腺癌细胞株存在多种蛋白差异分泌。MMP1对乳腺癌细胞转移侵袭有促进作用,可能是潜在的乳腺癌转移标志物。MMP1在促进癌症转移的过程中,与表达差异相比,分泌差异可能起主要促进作用。GRP75和MMP1存在相互作用,但GRP75对MMP1的作用可能不是影响MDA-MB-231HM细胞和MDA-MB-231细胞差异分泌MMP1的原因,而在乳腺癌细胞中CXCR4可能对MMP1表达存在调控作用。
Objective:To use human breast cancer cell lines with differently spontaneous lung metastatic capability as suitable models for the study of the molecular mechanisms related to breast cancer metastasis and finding out protein markers with metastatic potential.
Methods:MDA-MB-231HM was identified as one kind of cell lines derived from parental MDA-MB-231 cells by analyzing the karyotype of the MDA-MB-231HM cells with Giemsa chromosome banding stain.Then metastatic potential of both cell lines was tested in vitro by transwell and in vivo by comparing the weight of orthotopic tumor and the number of metastasis.Using two-dimensional electrophoresis(2-DE),we performed a proteomic comparison of both cell lines. Subsequently differentially expressed protein spots were identified by mass spectrometry.Differential expression was confirmed by Western blotting analysis and immunohistochemistry.
Results:All the MDA-MB-231HM cells exhibited X shaped chromosomes, which is completely different fromⅤshaped chromosomes of mice.Metastatic potential of MDA-MB-231HM cells was found higher than that of MDA-MB-231cells both in vitro and in vivo.We finally identified 14 unique proteins by proteomic analysis including Macrophage-capping protein(CapG),Galectin-1, Chloride intracellular channel protein 1,Endoplasmic reticulum protein ERp29 precursor,Transgelin-2,Peptidyl-prolyl cis-trans isomerase A(PPIase A),Stathmin-1 (STMN1),Isoform 1 of Uridine-cytidine kinase 2(UCK2),Rho GDP-dissociation inhibitor 2(ARHGDIB),Isocitrate dehydrogenase[NADP]cytoplasmic(IDH1), NDRG1 Protein NDRG1,Sperm protein associated with the nucleus on the X chromosome B/F,Neuron-specific calcium-binding hippocalcin,HSPA5 protein. Transgelin-2 and HSPA5 protein were down-regulated in MDA-MB-231HM cells, whereas Sperm protein associated with the nucleus on the x chromosome B/F and hippocalcin were only detected in MDA-MB-231 cells.CapG,Galectin-1,Chloride intracellular channel protein 1,ERp29,PPIase A,STMN1,UCK2,Rho GDP-dissociation inhibitor 2,Isocitrate dehydrogenase[NADP]cytoplasmic(IDH1) and NDRG1 were up-regulated in MDA-MB-231HM cells.Change of CapG,STMN1 and transgelin-2 was confirmed by western blotting analysis.Immunohistochemical analysis showed transgelin-2 expression was higher correlation in lymph node-negative tissues(19/30) and lower correlation in lymph node-positive tissues (5/30).
Conclusions:MDA-MB-231HM,a human breast carcinoma cell line with high capability of spontaneous lung metastasis,was a good tool for the study of breast cancer metastasis.Fourteen unique proteins in our study can both reveal molecular mechanisms related to breast cancer metastasis and be used as biological markers with metastatic potential for clinical diagnosis in breast cancer metastasis.
Objective:To compare the secretome of both human breast cancer cell lines with differently spontaneous lung metastatic capability for finding out biological markers with metastatic potential for clinical diagnosis in breast cancer metastasis. Further more,to study the regulation of the protein differently secreted by MDA-MB-231HM cells and MDA-MB-231 cells.
Methods:MDA-MB-231HM cells and MDA-MB-231 cells were cultured in serum-free medium for 24 hours,and the culture supernant of cells was desalted and concentrated by ultrafiltration to prepare the total secreted proteins.Two-dimensional gel electrophoresis(2-DE) was used to separate the secreted proteins.The differently secreted protein spots gels were identified by desorption/ionization time-of-flight mass spectrometry(MALDI-TOF-MS) and bioinformatics.Western blot and RT-PCR were used to further confirm differential expression and secretion of matrix metalloproteinase 1(MMP1).The expression vector of MMP1 specific shRNA(short hairpin RNA) and negative shRNA in vitro were constructed and transfected into MDA-MB-231 cells by lipofectamine2000 for the study of the function of MMP1 related to metastasis.The potential of invasion in vitro was tested by Transwell experiment.When MMP1 was immunoprecipitated by anti-MMP1 antibody for the study of the secretory regulation of MMP1,components from immunoprecipitated complex was separated by SDS-polyaerylamide gel electrophoresis and then identified by mass spectrometry.Interaction of MMP1 and GRP75 from immunoprecipitated complex was studied by confocalmicroscopy and co-immunoprecipitation.CXCR4 antagonist AMD3100 was used to interfere T47D cells,MDA-MB-231HM cells and MDA-MB-231 cells to study whether CXCR4 can affect the expressive regulation of MMP1.
Results:The secretory protein profiles reveal 22 proteins differently secreted by MDA-MB-231HM cells and MDA-MB-231 cells,whereas only five protein spots were identified by MALDI-TOF-MS including pro-MMP1,mature-MMP1,TIMP-2, TCTP,beta-2 microglobulin.MMP1 and TCTP were up-regulated in MDA-MB-231HM cells,whereas TIMP-2 and beta-2 microglobulin were up-regulated in MDA-MB-231 cells.Up-regulated expression and secretion of MMP1 were confirmed by western blot and RT-PCR,which also revealed secretory difference of both cell lines was more significant than expressive difference of both cell lines.Transwell experiment revealed that the number of MDA-MB-231 cells into which were transfected by the vector of MMP1 specific shRNA for 36 hours to penetrate polycarbonates coated with Matrigel was significantly lower than that of MDA-MB-231 cells into which were transfected by the vector of MMP1 negative shRNA for 36 hours.GRP75 was identified in immunoprecipitated complex.When MMP1 was immunoprecipitated by anti-MMP1 antibody,MMP1 was identified by western blotting with anti-MMP1 antibody from immunoprecipitated complex. Co-localization of GRP75 and MMP1 was determined by confocalmicroscopy, whereas western blot revealed there was no differently expressive amount of GRP75 between MDA-MB-231 cells and MDA-MB-231HM cells.AMD3100 can down-regulated the expression of MMP1 in T47D cells,MDA-MB-231HM cells and MDA-MB-231 cells.
Conclusions:Many kinds of secretory proteins were differently secreted from both human breast cancer cell lines with differently spontaneous lung metastatic capability.MMP1 may contribute to breast cancer metastasis and be used as a potential protein marker related to breast cancer metastasis.Contrasted with differently internal expression of MMP1 between the interior of MDA-MB-231 cells and MDA-MB-231HM cells,differently secretion of MMP1 between MDA-MB-231 cells and MDA-MB-231HM cells may play a predominant role in enhancing metastatic potential.GRP75 can interact with MMP1,whereas this kind of interaction may not be the effect of different secretion of MMP1 between MDA-MB-231 cells and MDA-MB-231HM cells.CXCR4 may regulate the expression of MMP1 in breast cancer cells.
引文
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