B-Myb基因在肺癌中的作用及分子机制的研究
发布时间：2018-07-16 18:05
【摘要】：B-Myb是高度保守的转录因子Myb家族的成员之一,在有增殖能力的细胞中普遍表达,并在细胞周期进程中起到重要作用。有研究发现,B-Myb在很多癌症细胞中高表达,如乳腺癌、肝细胞癌、神经母细胞瘤等。这提示我们,B-Myb在癌症的发生发展过程中可能发挥重要作用。迄今为止,B-Myb在肺癌中的表达及其作用机制尚不明确,故本论文主要研究B-Myb在肺癌组织样本中的表达水平及其对肺癌细胞增殖、迁移侵袭、肿瘤形成的影响,并探究其分子机制。第一部分B-Myb过表达对肺癌细胞增殖、迁移侵袭及肿瘤形成的影响及机制研究目的:1.研究B-Myb在肺癌组织中表达与肿瘤的临床病理特征之间的关系。2.检测B-Myb过表达对肺癌细胞增殖、细胞周期、迁移侵袭、肿瘤形成的影响。3.初步阐明B-Myb过表达促进肺癌细胞增殖、迁移侵袭及肿瘤形成的分子机制。方法:1.采用q RT-PCR、western blot及IHC检测肺癌组织和正常肺组织中B-Myb的表达水平,统计分析B-Myb在肺癌组织中表达与肿瘤的临床病理特征之间的关系。2.采用慢病毒感染的方法将目的基因B-Myb转染到肺癌细胞中,建立B-Myb过表达的细胞模型;q RT-PCR和western blot检测B-Myb及靶基因的m RNA和蛋白的表达;CCK-8检测细胞增殖;FCM检测细胞周期;划痕实验和Transwell检测细胞迁移侵袭;裸鼠成瘤实验检测肺癌细胞体内成瘤能力。3.RNA-seq检测肺癌细胞系H1299的B-Myb过表达组样本与对照组样本,GO富集分析和pathway富集分析筛选差异表达的基因及相关的信号通路。结果:1.检测40例肺癌患者和7例对照正常肺组织c DNA芯片中B-Myb的m RNA表达水平,并通过IHC检测69例肺癌患者及3例正常肺组织芯片中B-Myb的蛋白表达水平。统计分析显示,肺癌组织中B-Myb的m RNA和蛋白表达水平均显著高于正常肺组织,B-Myb的蛋白表达主要定位在细胞质内,且B-Myb的表达量与肿瘤的大小、淋巴结转移以及转移癌等密切相关。进一步检测肺癌6个细胞系H1299、A549、H157、H446、H524和H460中B-Myb的m RNA表达水平,结果发现在肺癌细胞H1299和A549中B-Myb的m RNA表达相对较低。2.肺癌细胞系H1299和A549的B-Myb过表达细胞模型成功建立,且过表达组较对照组的目的基因B-Myb表达量至少高出4倍;CCK-8结果显示,B-Myb过表达促进肺癌细胞的增殖;FCM检测结果显示,B-Myb过表达组较对照组S期细胞数量显著增加,且G1期细胞数量显著减少;划痕实验和Transwell迁移实验结果显示,B-Myb过表达促进肺癌细胞迁移;Transwell侵袭结果显示,B-Myb过表达促进肺癌细胞侵袭;体内实验结果显示,B-Myb过表达促进肺癌细胞的肿瘤形成。3.RNA-seq的检测和分析结果显示,B-Myb过表达诱导390个基因的差异表达,其中表达上调的有300个基因,表达下调的有90个基因。GO富集分析结果显示差异表达的基因功能主要与细胞外基质、生长因子、细胞发育进程有关。pathway富集分析结果显示主要的信号通路包括细胞粘附因子通路、PI3K-Akt信号通路、癌症通路及Ras信号通路。我们对部分差异表达的基因CCNA1、COL11A1、COL6A1、FN1、MMP2、NID1、FLT4、SPARC、INSR、IDH2、PDK3和IGFBP3进行q RT-PCR检测,差异表达的趋势与RNA-seq数据分析结果一致。进一步western blot分析显示,B-Myb过表达显著提高ERK和Akt磷酸化水平,能够激活ERK和Akt信号通路。结论:1.肺癌组织中B-Myb的m RNA水平和蛋白水平显著高于正常肺组织,B-Myb的蛋白表达主要定位在细胞质内,且B-Myb的表达量与肿瘤的大小、淋巴结转移以及转移癌等密切相关。2.体外实验显示,B-Myb过表达能够促进细胞的增殖、细胞周期进程和迁移侵袭;体内实验显示,B-Myb过表达能够提高肺癌细胞的肿瘤形成能力。3.RNA-seq检测分析结果显示,差异表达的基因功能主要与细胞外基质、生长因子、细胞发育进程有关,对部分差异表达的基因进行q RT-PCR检测,差异表达的趋势与RNA-seq数据分析结果一致,pathway富集分析结果显示主要的信号通路包括细胞粘附因子通路、PI3K-Akt信号通路、癌症通路及Ras信号通路。Western blot分析显示,B-Myb过表达显著提高ERK和Akt磷酸化水平,能够激活ERK和Akt信号通路,B-Myb能够促进肺癌的发生发展,或许部分是通过对ERK和Akt信号通路进行调节。第二部分B-Myb干扰对肺癌细胞增殖、迁移侵袭及肿瘤形成的影响及机制研究目的:1.检测B-Myb干扰对肺癌细胞增殖、周期、迁移侵袭、肿瘤形成等功能的影响。2.初步阐明B-Myb干扰抑制肺癌细胞增殖、迁移侵袭及肿瘤形成的分子机制。方法:1.采用慢病毒感染和瞬时转染的方法将目的基因B-Myb的干扰序列转染到肺癌细胞中,建立B-Myb干扰的细胞模型;q RT-PCR和western blot检测B-Myb及靶基因的m RNA和蛋白的表达;CCK-8检测细胞增殖;FCM检测细胞周期;划痕和Transwell检测细胞迁移侵袭;裸鼠成瘤检测体内成瘤能力。2.RNA-seq检测H1299的B-Myb干扰组与对照组样本,GO富集分析和pathway富集分析筛选出差异表达的基因及相关的信号通路。结果:1.肺癌细胞H1299和A549的B-Myb干扰模型成功建立,且B-Myb干扰效率大于60%;CCK-8结果显示,B-Myb干扰抑制肺癌细胞的增殖;FCM检测结果显示,肺癌细胞B-Myb干扰后S期细胞数量减少,且G1期细胞数量显著增加;划痕和Transwell迁移结果显示,B-Myb干扰抑制肺癌细胞迁移;Transwell侵袭结果显示,B-Myb干扰抑制肺癌细胞侵袭;体内实验结果显示,B-Myb干扰抑制肺癌细胞的肿瘤形成。2.RNA-seq的检测和分析结果显示,B-Myb干扰诱导13362个基因差异表达,其中包括6343个基因表达上调,7019个基因表达下调。GO富集分析显示差异表达的基因主要参与调控细胞信号转导、细胞周期、细胞增殖、细胞凋亡及迁移侵袭等功能,Pathway富集分析的主要是MAPK信号通路、凋亡和细胞周期相关信号通路。我们对部分差异表达的基因COL11A1、FLT4、SPARC、IDH2、PDK3和IGFBP3进行q RT-PCR检测,差异表达的趋势与RNA-seq数据分析结果一致。结论:1.体外实验显示,B-Myb干扰能够抑制肺癌细胞的增殖、迁移侵袭、且S期细胞减少;体内实验显示,B-Myb干扰能够降低肺癌细胞的肿瘤形成能力。2.RNA-seq检测并分析显示,细胞外基质、生长因子、细胞发育进程都存在基因表达的不同程度的下调。对部分差异表达的基因进行q RT-PCR检测,差异表达的趋势与RNA-seq数据分析结果一致,pathway富集分析结果显示,主要的信号通路包括MAPK信号通路、凋亡和细胞周期相关信号通路。
[Abstract]:B-Myb is a member of the highly conserved transcription factor Myb family and is widely expressed in proliferating cells and plays an important role in the process of cell cycle. Some studies have found that B-Myb is highly expressed in many cancer cells, such as breast cancer, hepatocellular carcinoma, and neuroblastoma. This suggests that B-Myb is in the development of cancer. So far, the expression and mechanism of B-Myb in lung cancer are not clear. Therefore, this paper mainly studies the expression level of B-Myb in lung cancer tissue samples and its effect on lung cancer cell proliferation, migration and invasion, tumor formation, and explore its molecular mechanism. The first part of B-Myb overexpression on lung cancer The effect and mechanism of cell proliferation, migration, invasion and tumor formation: 1. study the relationship between the expression of B-Myb in lung cancer tissue and the clinicopathological features of tumor.2. detection of B-Myb overexpression on the proliferation, cell cycle, migration and invasion, and the effect of.3. on the proliferation of lung cancer cells and promoting the proliferation of lung cancer cells, migration and migration of lung cancer cells The molecular mechanism of invasion and tumor formation. Methods: 1. the expression of B-Myb in lung cancer tissues and normal lung tissues was detected by Q RT-PCR, Western blot and IHC. The relationship between the expression of B-Myb in lung cancer tissues and the clinicopathological features of the tumor was statistically analyzed.2. using the lentivirus infection method to transfect the target gene B-Myb to lung cancer. In the cell, B-Myb overexpressed cell model was established; Q RT-PCR and Western blot were used to detect the expression of M RNA and protein of B-Myb and target genes; CCK-8 detection of cell proliferation; FCM detection of cell cycle; scratch test and Transwell detection of cell migration and invasion; nude mice tumor testing detection of lung cancer cells in vivo tumorigenicity.3.RNA-seq detection of lung cancer cell lines 99 B-Myb overexpressed group samples and control group samples, GO enrichment analysis and pathway enrichment analysis were used to screen differentially expressed genes and related signaling pathways. Results: 1. detection of M RNA expression level of B-Myb in 40 cases of lung cancer patients and 7 normal lung tissue C DNA chips, and 69 cases of lung cancer and 3 normal lung tissue chips by IHC The protein expression level of middle B-Myb showed that the expression level of M RNA and protein of B-Myb in lung cancer tissues was significantly higher than that of normal lung tissue. The protein expression of B-Myb was mainly located in the cytoplasm, and the expression of B-Myb was closely related to the size of tumor, lymph node metastasis and metastatic carcinoma. Further detection of the 6 cell line of lung cancer H12 99, A549, H157, H446, H524 and H460 B-Myb m RNA expression level. The results showed that B-Myb M protein expression in lung cancer cells H1299 and A549 was relatively low, and the overexpressed cell model was successfully established, and the overexpressed group was at least 4 times higher than the control group. The expression of overexpression promoted the proliferation of lung cancer cells, and the results of FCM detection showed that the number of S phase cells in the B-Myb overexpression group was significantly increased and the number of G1 cells decreased significantly. The results of scratch test and Transwell migration showed that B-Myb overexpression promoted the migration of lung cancer cells; the result of Transwell invasion showed that the over expression of B-Myb promoted lung cancer cells. The results of the in vivo experiment showed that B-Myb overexpression promoted the tumor formation of.3.RNA-seq in lung cancer cells. The results showed that B-Myb overexpression induced the differential expression of 390 genes, of which 300 genes were up-regulated, and 90 gene.GO enrichment analysis showed that the function of differentially expressed genes was mainly related to the expression of down regulation. The results of extracellular matrix, growth factor, and cell development related to.Pathway enrichment analysis showed that the main signaling pathways included cell adhesion factor pathway, PI3K-Akt signaling pathway, cancer pathway and Ras signaling pathway. We expressed genes CCNA1, COL11A1, COL6A1, FN1, MMP2, NID1, FLT4, SPARC, INSR, INSR, INSR, INSR, SPARC, and CCNA1 The trend of differential expression was consistent with the results of RNA-seq data analysis. Further western blot analysis showed that B-Myb overexpression significantly increased the level of phosphorylation of ERK and Akt, and could activate ERK and Akt signaling pathways. Conclusion: 1. the B-Myb M levels and protein levels in lung cancer tissues are significantly higher than those of normal lung tissues. The protein expression of 1. lung cancer tissues is significantly higher than that of normal lung tissue. It is mainly located in the cytoplasm, and the expression of B-Myb is closely related to the size of tumor, lymph node metastasis and metastatic carcinoma. In vitro,.2. experiments show that overexpression of B-Myb can promote cell proliferation, cell cycle process and migration invasion. In vivo experiments show that B-Myb overexpression can improve the tumor formation ability of lung cancer cells.3.RNA-seq The results of detection analysis showed that the differentially expressed gene functions were mainly related to extracellular matrix, growth factor, cell development process, and Q RT-PCR detection for some differentially expressed genes. The trend of differential expression was consistent with the results of RNA-seq data analysis. Pathway enrichment analysis showed that the main signal pathways included cell adhesion factors. The pathway, PI3K-Akt signaling pathway, cancer pathway and Ras signaling pathway.Western blot analysis showed that B-Myb overexpression significantly increased the level of ERK and Akt phosphorylation, activated ERK and Akt signaling pathways, and B-Myb could promote the development of lung cancer, perhaps partly through the regulation of ERK and Akt signaling pathways. The second part interferes with lung cancer. Effects and mechanisms of cell proliferation, migration and invasion and tumor formation: 1. detection of the effects of B-Myb interference on proliferation, cycle, migration and invasion, and tumor formation of lung cancer cells..2. preliminarily clarifies the molecular mechanism of B-Myb interference to inhibit the proliferation, migration and invasion of lung cancer cells and the formation of tumor. Methods 1. use lentivirus infection and transient transformation. The staining method transfected the interference sequence of the target gene B-Myb into the lung cancer cells and established the B-Myb interference cell model; Q RT-PCR and Western blot detected the B-Myb and the expression of M RNA and protein of the target gene; CCK-8 detection of cell proliferation; FCM detection of cell cycle; scratch and Transwell detection of cell migration and invasion; tumor formation detection in nude mice. .2.RNA-seq detection of H1299 B-Myb interference group and control group samples, GO enrichment analysis and pathway enrichment analysis screened differentially expressed genes and related signaling pathways. Results: 1. the B-Myb interference model of H1299 and A549 in lung cancer cells was successfully established, and B-Myb interference efficiency was more than 60%; CCK-8 results showed that B-Myb interference inhibited lung cancer cells. The results of FCM detection showed that the number of S cells decreased and the number of G1 cells increased significantly after B-Myb interference, and the results of scratch and Transwell migration showed that B-Myb interference inhibited the migration of lung cancer cells; the results of Transwell invasion showed that B-Myb interference inhibited the invasion of lung cancer cells; in vivo experimental results showed that B-Myb interference inhibited lung cancer. The detection and analysis of the tumor formation of.2.RNA-seq showed that B-Myb interference induced 13362 differentially expressed genes, including 6343 gene expression up-regulated, 7019 gene expression down-regulation.GO enrichment analysis showed that the differentially expressed genes were mainly involved in regulating cell signal transduction, cell cycle, cell proliferation, cell apoptosis and migration invasion. MAPK signaling pathway, apoptosis and cell cycle related signal pathways were mainly analyzed by Pathway enrichment analysis. We detected Q RT-PCR in some differentially expressed genes COL11A1, FLT4, SPARC, IDH2, PDK3 and IGFBP3. The trend of differential expression was consistent with that of RNA-seq data analysis. Conclusion: 1. in vitro experiments showed that B-Myb interference could be suppressed. The proliferation, migration and invasion of lung cancer cells and the decrease of S phase cells; in vivo experiments showed that B-Myb interference could reduce the tumor formation ability of lung cancer cells by.2.RNA-seq detection and analysis showed that extracellular matrix, growth factor, and cell development process were all down regulated by different levels of gene expression. Q RT- for some differentially expressed genes PCR detection, the trend of differential expression is consistent with the results of RNA-seq data analysis. The results of pathway enrichment analysis show that the main signaling pathways include MAPK signaling pathway, apoptosis and cell cycle related signaling pathways.
【学位授予单位】：重庆医科大学
【学位级别】：博士
【学位授予年份】：2017
【分类号】：R734.2
本文编号：2127197
[Abstract]:B-Myb is a member of the highly conserved transcription factor Myb family and is widely expressed in proliferating cells and plays an important role in the process of cell cycle. Some studies have found that B-Myb is highly expressed in many cancer cells, such as breast cancer, hepatocellular carcinoma, and neuroblastoma. This suggests that B-Myb is in the development of cancer. So far, the expression and mechanism of B-Myb in lung cancer are not clear. Therefore, this paper mainly studies the expression level of B-Myb in lung cancer tissue samples and its effect on lung cancer cell proliferation, migration and invasion, tumor formation, and explore its molecular mechanism. The first part of B-Myb overexpression on lung cancer The effect and mechanism of cell proliferation, migration, invasion and tumor formation: 1. study the relationship between the expression of B-Myb in lung cancer tissue and the clinicopathological features of tumor.2. detection of B-Myb overexpression on the proliferation, cell cycle, migration and invasion, and the effect of.3. on the proliferation of lung cancer cells and promoting the proliferation of lung cancer cells, migration and migration of lung cancer cells The molecular mechanism of invasion and tumor formation. Methods: 1. the expression of B-Myb in lung cancer tissues and normal lung tissues was detected by Q RT-PCR, Western blot and IHC. The relationship between the expression of B-Myb in lung cancer tissues and the clinicopathological features of the tumor was statistically analyzed.2. using the lentivirus infection method to transfect the target gene B-Myb to lung cancer. In the cell, B-Myb overexpressed cell model was established; Q RT-PCR and Western blot were used to detect the expression of M RNA and protein of B-Myb and target genes; CCK-8 detection of cell proliferation; FCM detection of cell cycle; scratch test and Transwell detection of cell migration and invasion; nude mice tumor testing detection of lung cancer cells in vivo tumorigenicity.3.RNA-seq detection of lung cancer cell lines 99 B-Myb overexpressed group samples and control group samples, GO enrichment analysis and pathway enrichment analysis were used to screen differentially expressed genes and related signaling pathways. Results: 1. detection of M RNA expression level of B-Myb in 40 cases of lung cancer patients and 7 normal lung tissue C DNA chips, and 69 cases of lung cancer and 3 normal lung tissue chips by IHC The protein expression level of middle B-Myb showed that the expression level of M RNA and protein of B-Myb in lung cancer tissues was significantly higher than that of normal lung tissue. The protein expression of B-Myb was mainly located in the cytoplasm, and the expression of B-Myb was closely related to the size of tumor, lymph node metastasis and metastatic carcinoma. Further detection of the 6 cell line of lung cancer H12 99, A549, H157, H446, H524 and H460 B-Myb m RNA expression level. The results showed that B-Myb M protein expression in lung cancer cells H1299 and A549 was relatively low, and the overexpressed cell model was successfully established, and the overexpressed group was at least 4 times higher than the control group. The expression of overexpression promoted the proliferation of lung cancer cells, and the results of FCM detection showed that the number of S phase cells in the B-Myb overexpression group was significantly increased and the number of G1 cells decreased significantly. The results of scratch test and Transwell migration showed that B-Myb overexpression promoted the migration of lung cancer cells; the result of Transwell invasion showed that the over expression of B-Myb promoted lung cancer cells. The results of the in vivo experiment showed that B-Myb overexpression promoted the tumor formation of.3.RNA-seq in lung cancer cells. The results showed that B-Myb overexpression induced the differential expression of 390 genes, of which 300 genes were up-regulated, and 90 gene.GO enrichment analysis showed that the function of differentially expressed genes was mainly related to the expression of down regulation. The results of extracellular matrix, growth factor, and cell development related to.Pathway enrichment analysis showed that the main signaling pathways included cell adhesion factor pathway, PI3K-Akt signaling pathway, cancer pathway and Ras signaling pathway. We expressed genes CCNA1, COL11A1, COL6A1, FN1, MMP2, NID1, FLT4, SPARC, INSR, INSR, INSR, INSR, SPARC, and CCNA1 The trend of differential expression was consistent with the results of RNA-seq data analysis. Further western blot analysis showed that B-Myb overexpression significantly increased the level of phosphorylation of ERK and Akt, and could activate ERK and Akt signaling pathways. Conclusion: 1. the B-Myb M levels and protein levels in lung cancer tissues are significantly higher than those of normal lung tissues. The protein expression of 1. lung cancer tissues is significantly higher than that of normal lung tissue. It is mainly located in the cytoplasm, and the expression of B-Myb is closely related to the size of tumor, lymph node metastasis and metastatic carcinoma. In vitro,.2. experiments show that overexpression of B-Myb can promote cell proliferation, cell cycle process and migration invasion. In vivo experiments show that B-Myb overexpression can improve the tumor formation ability of lung cancer cells.3.RNA-seq The results of detection analysis showed that the differentially expressed gene functions were mainly related to extracellular matrix, growth factor, cell development process, and Q RT-PCR detection for some differentially expressed genes. The trend of differential expression was consistent with the results of RNA-seq data analysis. Pathway enrichment analysis showed that the main signal pathways included cell adhesion factors. The pathway, PI3K-Akt signaling pathway, cancer pathway and Ras signaling pathway.Western blot analysis showed that B-Myb overexpression significantly increased the level of ERK and Akt phosphorylation, activated ERK and Akt signaling pathways, and B-Myb could promote the development of lung cancer, perhaps partly through the regulation of ERK and Akt signaling pathways. The second part interferes with lung cancer. Effects and mechanisms of cell proliferation, migration and invasion and tumor formation: 1. detection of the effects of B-Myb interference on proliferation, cycle, migration and invasion, and tumor formation of lung cancer cells..2. preliminarily clarifies the molecular mechanism of B-Myb interference to inhibit the proliferation, migration and invasion of lung cancer cells and the formation of tumor. Methods 1. use lentivirus infection and transient transformation. The staining method transfected the interference sequence of the target gene B-Myb into the lung cancer cells and established the B-Myb interference cell model; Q RT-PCR and Western blot detected the B-Myb and the expression of M RNA and protein of the target gene; CCK-8 detection of cell proliferation; FCM detection of cell cycle; scratch and Transwell detection of cell migration and invasion; tumor formation detection in nude mice. .2.RNA-seq detection of H1299 B-Myb interference group and control group samples, GO enrichment analysis and pathway enrichment analysis screened differentially expressed genes and related signaling pathways. Results: 1. the B-Myb interference model of H1299 and A549 in lung cancer cells was successfully established, and B-Myb interference efficiency was more than 60%; CCK-8 results showed that B-Myb interference inhibited lung cancer cells. The results of FCM detection showed that the number of S cells decreased and the number of G1 cells increased significantly after B-Myb interference, and the results of scratch and Transwell migration showed that B-Myb interference inhibited the migration of lung cancer cells; the results of Transwell invasion showed that B-Myb interference inhibited the invasion of lung cancer cells; in vivo experimental results showed that B-Myb interference inhibited lung cancer. The detection and analysis of the tumor formation of.2.RNA-seq showed that B-Myb interference induced 13362 differentially expressed genes, including 6343 gene expression up-regulated, 7019 gene expression down-regulation.GO enrichment analysis showed that the differentially expressed genes were mainly involved in regulating cell signal transduction, cell cycle, cell proliferation, cell apoptosis and migration invasion. MAPK signaling pathway, apoptosis and cell cycle related signal pathways were mainly analyzed by Pathway enrichment analysis. We detected Q RT-PCR in some differentially expressed genes COL11A1, FLT4, SPARC, IDH2, PDK3 and IGFBP3. The trend of differential expression was consistent with that of RNA-seq data analysis. Conclusion: 1. in vitro experiments showed that B-Myb interference could be suppressed. The proliferation, migration and invasion of lung cancer cells and the decrease of S phase cells; in vivo experiments showed that B-Myb interference could reduce the tumor formation ability of lung cancer cells by.2.RNA-seq detection and analysis showed that extracellular matrix, growth factor, and cell development process were all down regulated by different levels of gene expression. Q RT- for some differentially expressed genes PCR detection, the trend of differential expression is consistent with the results of RNA-seq data analysis. The results of pathway enrichment analysis show that the main signaling pathways include MAPK signaling pathway, apoptosis and cell cycle related signaling pathways.
【学位授予单位】：重庆医科大学
【学位级别】：博士
【学位授予年份】：2017
【分类号】：R734.2
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