人参皂苷Rg3通过抑制WEE1激酶表达增加结肠癌细胞对DNA损伤药物的敏感性
发布时间：2018-07-26 12:20
【摘要】：背景结直肠癌是常见的消化道恶性肿瘤,其发病率居所有恶性肿瘤第三位,死亡率居所有恶性肿瘤第二位。人参皂苷Rg3是由人参中提取的活性成分,其可抑制肿瘤细胞的增殖、迁移和侵袭,并促进肿瘤细胞凋亡。WEE1蛋白是调控细胞周期G2检查点的重要基因,其表达变化可影响DNA损伤药物顺铂、紫杉醇、5-氟尿嘧啶等药物对细胞的杀伤作用。在胃癌和卵巢癌的研究中发现,人参皂苷可协同增敏顺铂和5-氟尿嘧啶对细胞的增殖抑制效应。然而,人参皂苷Rg3、DNA损伤药物和WEE1蛋白之间的作用并未见相关报道,本研究主要探讨三者之间的相互关系,探讨人参皂苷Rg3增敏DNA损伤药物的相关分子机制。第一部分人参皂苷Rg3通过抑制WEE1激酶表达增敏结肠癌对DNA损伤药物敏感性的机制研究研究目的探讨人参皂苷Rg3是否可影响结肠癌细胞对DNA损伤药物顺铂和5-氟尿嘧啶的增殖抑制效应及其机制。研究方法1.为了探讨人参皂苷Rg3联合DNA损伤药物顺铂或5-氟尿嘧啶对Wi Dr、SW948和COLO205等结肠癌细胞增殖活性的影响。应用CCK-8细胞增殖活性检测法,检测不同浓度人参皂苷Rg3联合不同浓度DNA损伤药物顺铂或5-氟尿嘧啶干预Wi Dr、SW948和COLO205三株结肠癌细胞后对其细胞增殖活性的影响。2.为了探讨人参皂苷Rg3影响结肠癌细胞增殖活性的潜在机制。应用q RT-PCR法检测不同浓度人参皂苷Rg3干预相同时间和相同浓度人参皂苷Rg3干预不同时间后结肠癌细胞内WEE1的表达水平变化。3.为了探讨WEE1过表达在人参皂苷Rg3影响结肠癌细胞对DNA损伤药物顺铂和5-氟尿嘧啶敏感性过程中的作用。首先应用质粒过表达技术对Wi Dr,SW948和COLO205等结肠癌细胞进行WEE1过表达,并应用q RT-PCR法检测过表达程度;其次应用CCK-8细胞增殖活性检测法检测10μM/L顺铂+75μM/L人参皂苷Rg3+不同pc DNA-WEE1浓度和3μM/L 5-氟尿嘧啶+50μM/L人参皂苷Rg3+不同pc DNA-WEE1浓度等处理对于结肠癌细胞增殖活力的影响。结果1.顺铂和5-氟尿嘧啶对于结肠癌细胞Wi Dr、SW948和COLO205等增殖活力的抑制成浓度依赖性增加;随着应用人参皂苷Rg3浓度(0μM/L、25μM/L、50μM/L、75μM/L)的增加,在应用相同浓度顺铂或5-氟尿嘧啶的前提下,Wi Dr,SW948和COLO205等结肠癌细胞的增殖活力逐渐降低;2.应用人参皂苷Rg3干预三株结肠癌细胞,随着人参皂苷Rg3干预浓度(0μM/L、25μM/L、50μM/L、75μM/L和100μM/L)的增加,Wi Dr、SW948和COLO205等结肠癌细胞中WEE1的表达明显降低;应用50μM/L人参皂苷Rg3干预三株结肠癌细胞,随着人参皂苷Rg3干预时间(0 h、6 h、12 h、18 h和24h)的增加,Wi Dr,SW948和COLO205等结肠癌细胞中WEE1的表达逐渐降低;3.应用pc DNA-WEE1质粒可在三株结肠癌细胞中成功上调WEE1的表达;在相同浓度顺铂(10μM/L)+人参皂苷Rg3(75μM/L)干预的前提下,随着pc DNA-WEE1质粒转染浓度(10 ng、50 ng、100 ng、150 ng)的增加,Wi Dr、SW948和COLO205等结肠癌细胞的增殖活力逐渐增加;在相同浓度5-氟尿嘧啶(3μM/L)+人参皂苷Rg3(50μM/L)干预的前提下,随着pc DNA-WEE1质粒转染浓度(10ng、50 ng、100 ng、150 ng)的增加,Wi Dr、SW948和COLO205等结肠癌细胞的增殖活力逐渐增加。结论1.人参皂苷Rg3可增敏DNA损伤药物(顺铂和5-氟尿嘧啶)对结肠癌细胞增殖活力的抑制效应;2.人参皂苷Rg3对WEE1表达的抑制效应呈浓度依赖性和时间依赖性增加;3.过表达WEE1可减弱人参皂苷Rg3增敏DNA损伤药物(顺铂和5-氟尿嘧啶)对结肠癌细胞增殖活力的抑制效应。第二部分WEE1在结直肠癌组织中的表达及临床病理意义分析研究目的探讨WEE1蛋白在结直肠癌中的表达与结直肠癌患者临床病理参数和预后的相关性。研究方法1.为了探讨WEE1在结直肠癌组织和癌旁组织中的表达,应用Western blot和q RT-PCR法检测新鲜结直肠癌组织和癌旁组织中WEE1的表达;2.为了明确WEE1蛋白在结直肠癌组织中的表达与结直肠癌患者临床病理资料的相关性。应用卡方检验分析WEE1蛋白的阴性表达和阳性表达与结直肠癌患者的年龄、性别、肿瘤部位、肿瘤直径、肿瘤分化程度、有无淋巴结转移、有无远处转移、血清CEA水平、有无腹膜转移、T分期、N分期、M分期及TNM分期等临床病理参数的相关性;3.为了探讨WEE1蛋白在结直肠癌组织中的表达与结直肠癌患者预后的相关性,应用Kaplan-Meier法绘制生存曲线,以Log-rank检验比较WEE1蛋白的阴性表达和阳性表达与患者预后的相关性;应用单因素和多因素Cox回归分析影响结直肠癌患者预后的危险因素。研究结果1.在33例结直肠癌患者病理标本中,18例患者的结直肠癌组织中,WEE1蛋白和m RNA呈高表达;而15例患者的结直肠癌组织中,WEE1蛋白和m RNA呈低表达;2.免疫组织化学结果示,在142例患者的石蜡包埋结直肠癌组织中,WEE1蛋白在86例中呈阳性表达,在56例中呈阴性表达;3.WEE1阳性表达与结直肠癌患者的肿瘤分化程度(P=0.033)、N分期(P=0.005)、TNM分期(P=0.009)、Duke’s分期(P=0.001)和淋巴结转移(P=0.006)等参数有明显相关性,结果具有统计学意义;4.根据WEE1蛋白表达水平,将所有结直肠癌患者分为阳性表达组和阴性表达组,WEE1阳性表达组患者的平均生存时间明显短于WEE1阴性表达组;单因素分析结果示,肿瘤大小(HR=0.5,95%置信区间0.263-0.949,P=0.034)、TNM分期(HR=1.402,95%置信区间0.934-6.176,P=0.012)、M分期(HR=1.562,95%置信区间0.231-4.685,P=0.002)、肝转移(HR=3.462,95%置信区间1.265-10.256,P=0.014)和WEE1表达(HR=7.608,95%置信区间3.019-19.185,P0.001)是影响结直肠癌患者预后的危险因素;多因素Cox比例风险回归模型结果示,TNM分期(HR=2.899,95%置信区间2.072-8.056,P0.001)和WEE1表达(HR=6.533,95%置信区间2.93-14.566,P0.001)是影响结直肠癌患者预后的独立危险因素。5.在I期结直肠癌患者中,WEE1的表达与患者OS和DFS并无明显相关性,而在II期和III期结直肠癌患者患者中,WEE1阳性表达提示患者OS和DFS较差。研究结论WEE1在结直肠癌组织中呈高表达;其阳性表达提示结直肠癌患者预后较差;WEE1阳性表达和TNM分期是影响结直肠癌患者预后的独立危险因素。
[Abstract]:Background colorectal cancer (CRC) is a common malignant tumor of the digestive tract, with the incidence of third of all malignant tumors and second of all malignant tumors. Ginsenoside Rg3 is the active ingredient extracted from ginseng, which can inhibit the proliferation, migration and invasion of tumor cells, and promote the apoptosis of tumor cell.WEE1 protein to regulate cell cycle G2 An important gene of the checkpoint, its expression changes can affect the killing effect of DNA damage drugs cisplatin, paclitaxel, 5- fluorouracil and other drugs on cells. In the study of gastric and ovarian cancer, ginsenoside can synergistically sensitized cisplatin and 5- fluorouracil to inhibit the proliferation of cells. However, ginsenoside Rg3, DNA damage drugs and WEE1 eggs The role of white is not reported. This study mainly discusses the relationship between the three and probes into the molecular mechanism of ginsenoside Rg3 sensitized DNA damage drug. Part 1. The mechanism of ginsenoside Rg3 by inhibiting the expression of WEE1 kinase to sensitist colon cancer to DNA damage drug sensitivity and study the objective of ginsenoside Rg3 Whether it can affect the proliferation inhibition effect of colon cancer cells on DNA damaged cisplatin and 5- fluorouracil and its mechanism. 1. in order to investigate the effect of ginsenoside Rg3 combined with DNA damaged cisplatin or 5- fluorouracil on the proliferation of Wi Dr, SW948 and COLO205 and other colon cancer cells. Detection of CCK-8 cell proliferation activity, detection method, detection Different concentrations of ginsenoside Rg3 combined with different concentrations of DNA injury drugs cisplatin or 5- fluorouracil in Wi Dr, SW948 and COLO205 three colon cancer cells effect on the cell proliferation activity.2. in order to explore the potential mechanism of ginsenoside Rg3 to influence the proliferation of colon cancer cells. The Q RT-PCR method was used to detect different concentrations of ginsenoside Rg3 dry Changes in the expression level of WEE1 in colon cancer cells after the intervention of the same time and the same concentration of ginsenoside Rg3 in order to explore the effect of WEE1 overexpression on Ginsenoside Rg3 effect on the sensitivity of colon cancer cells to DNA damaged cisplatin and 5- fluorouracil. First, the plasmid overexpression technique should be used for Wi Dr, SW948 and COLO. 205 of the colon cancer cells were overexpressed by WEE1, and the degree of overexpression was detected by Q RT-PCR method. Secondly, the CCK-8 cell proliferation activity detection method was used to detect the concentration of different PC DNA-WEE1 of cisplatin +75 mu M/L and 3 mu M/L 5- fluorouracil (3 mu M/L 5- fluorouracil). Results 1. cisplatin and 5- fluorouracil increased the inhibitory effect on the proliferation of Wi Dr, SW948 and COLO205 in colon cancer cells. With the increase of the concentration of ginsenoside Rg3 (0 M/L, 25 u M/L, 50 u M/L, 75 micron M/L), under the premise of the application of the same concentration of cisplatin or 5- fluorouracil, Wi The proliferation activity of colon cancer cells decreased gradually; 2. the expression of ginsenoside Rg3 in three colon cancer cells was significantly reduced with the increase of ginsenoside Rg3 intervention concentration (0 mu M/L, 25 mu M/L, 50 mu M/L, 75 mu M/L and 100 mu M/L), and the expression of WEE1 was significantly reduced in Wi Dr, SW948 and COLO205 colon cancer cells, and three colon cancer was interfered with 50 micronosides of ginsenoside. Cells, with the increase of ginsenoside Rg3 intervention time (0 h, 6 h, 12 h, 18 h and 24h), the WEE1 expression in Wi Dr, SW948, COLO205 and other colon cancer cells gradually decreased; 3. application of PC plasmid could successfully increase the expression in three colon cancer cells, under the premise of the intervention of the same concentration of cisplatin (10 mu) + ginsenoside (75 mu). With the increase of the transfection concentration of PC DNA-WEE1 plasmids (10 ng, 50 ng, 100 ng, 150 ng), the proliferation activity of Wi Dr, SW948, COLO205 and other colon cancer cells gradually increased. The proliferation activity of colon cancer cells such as 948 and COLO205 increased gradually. Conclusion 1. ginsenoside Rg3 can increase the inhibitory effect of DNA injury drugs (cisplatin and 5- fluorouracil) on the proliferation of colon cancer cells; 2. the inhibitory effect of ginsenoside Rg3 on WEE1 expression is concentration dependent and time dependent; 3. over expression of WEE1 can weaken ginseng soap. The inhibitory effect of glucoside Rg3 sensitized DNA damage drugs (cisplatin and 5- fluorouracil) on the proliferation of colon cancer cells. Second the expression and clinicopathological significance of part WEE1 in colorectal cancer tissue and its clinicopathological significance study on the correlation between the expression of WEE1 protein in colorectal cancer and the clinicopathological parameters and prognosis of colorectal cancer patients. Method 1. in order to investigate the expression of WEE1 in colorectal cancer tissue and para cancer tissue, the expression of WEE1 in fresh colorectal cancer tissues and adjacent tissues was detected by Western blot and Q RT-PCR. 2. in order to clarify the correlation between the expression of WEE1 protein in colorectal cancer tissue and the clinical data of colorectal cancer patients, chi square test analyzed WE. The negative expression and positive expression of E1 protein were related to the age, sex, tumor site, tumor location, tumor diameter, tumor differentiation, lymph node metastasis, distant metastasis, serum CEA level, T stage, N staging, M staging, TNM staging and other clinicopathological parameters; 3. The correlation between the expression of colorectal cancer and the prognosis of colorectal cancer patients. The survival curve was drawn by Kaplan-Meier method. The correlation between the negative expression and positive expression of WEE1 protein and the prognosis of the patients was compared with the Log-rank test. The risk factors affecting the prognosis of the patients with colorectal cancer were analyzed by single factor and multiple factor Cox regression analysis. 1. In 33 cases of colorectal cancer, 18 cases of colorectal cancer tissues, WEE1 protein and m RNA were highly expressed, while 15 cases of colorectal cancer tissues, WEE1 protein and m RNA were low expression; 2. immunohistochemical results showed that in 142 cases of paraffin embedded colorectal cancer tissues, the WEE1 protein was positive in 86 cases. Negative expression was found in 56 cases, and 3.WEE1 positive expression was significantly correlated with tumor differentiation (P=0.033), N staging (P=0.005), TNM staging (P=0.009), Duke 's staging (P=0.001) and lymph node metastasis (P=0.006), and the results were statistically significant. 4. according to the level of WEE1 protein expression, all patients with colorectal cancer were expressed. The average survival time of the WEE1 positive group was significantly shorter than that of the WEE1 negative expression group, and the single factor analysis showed that the tumor size (HR=0.5,95% confidence interval 0.263-0.949, P=0.034), TNM staging (HR=1.402,95% confidence interval 0.934-6.176, P=0.012), M stages (HR=1.562,95% confidence interval 0.231-4.685, HR=1.562,95%) =0.002), liver metastases (HR=3.462,95% confidence interval 1.265-10.256, P=0.014) and WEE1 expression (HR=7.608,95% confidence interval 3.019-19.185, P0.001) are the risk factors affecting the prognosis of colorectal cancer patients. The multifactor Cox proportional risk regression model results show that TNM stages (HR= 2.899,95% confidence interval) and expressions are expressed. 2.93-14.566, P0.001) is an independent risk factor affecting the prognosis of colorectal cancer patients.5. in I patients with colorectal cancer, the expression of WEE1 is not associated with the patients' OS and DFS, but in patients with II and III, WEE1 positive expression suggests that OS and DFS are poor. The positive expression indicates that the prognosis of patients with colorectal cancer is poor. WEE1 positive expression and TNM stage are independent risk factors for prognosis of colorectal cancer.
【学位授予单位】：郑州大学
【学位级别】：博士
【学位授予年份】：2016
【分类号】：R735.35
[Abstract]:Background colorectal cancer (CRC) is a common malignant tumor of the digestive tract, with the incidence of third of all malignant tumors and second of all malignant tumors. Ginsenoside Rg3 is the active ingredient extracted from ginseng, which can inhibit the proliferation, migration and invasion of tumor cells, and promote the apoptosis of tumor cell.WEE1 protein to regulate cell cycle G2 An important gene of the checkpoint, its expression changes can affect the killing effect of DNA damage drugs cisplatin, paclitaxel, 5- fluorouracil and other drugs on cells. In the study of gastric and ovarian cancer, ginsenoside can synergistically sensitized cisplatin and 5- fluorouracil to inhibit the proliferation of cells. However, ginsenoside Rg3, DNA damage drugs and WEE1 eggs The role of white is not reported. This study mainly discusses the relationship between the three and probes into the molecular mechanism of ginsenoside Rg3 sensitized DNA damage drug. Part 1. The mechanism of ginsenoside Rg3 by inhibiting the expression of WEE1 kinase to sensitist colon cancer to DNA damage drug sensitivity and study the objective of ginsenoside Rg3 Whether it can affect the proliferation inhibition effect of colon cancer cells on DNA damaged cisplatin and 5- fluorouracil and its mechanism. 1. in order to investigate the effect of ginsenoside Rg3 combined with DNA damaged cisplatin or 5- fluorouracil on the proliferation of Wi Dr, SW948 and COLO205 and other colon cancer cells. Detection of CCK-8 cell proliferation activity, detection method, detection Different concentrations of ginsenoside Rg3 combined with different concentrations of DNA injury drugs cisplatin or 5- fluorouracil in Wi Dr, SW948 and COLO205 three colon cancer cells effect on the cell proliferation activity.2. in order to explore the potential mechanism of ginsenoside Rg3 to influence the proliferation of colon cancer cells. The Q RT-PCR method was used to detect different concentrations of ginsenoside Rg3 dry Changes in the expression level of WEE1 in colon cancer cells after the intervention of the same time and the same concentration of ginsenoside Rg3 in order to explore the effect of WEE1 overexpression on Ginsenoside Rg3 effect on the sensitivity of colon cancer cells to DNA damaged cisplatin and 5- fluorouracil. First, the plasmid overexpression technique should be used for Wi Dr, SW948 and COLO. 205 of the colon cancer cells were overexpressed by WEE1, and the degree of overexpression was detected by Q RT-PCR method. Secondly, the CCK-8 cell proliferation activity detection method was used to detect the concentration of different PC DNA-WEE1 of cisplatin +75 mu M/L and 3 mu M/L 5- fluorouracil (3 mu M/L 5- fluorouracil). Results 1. cisplatin and 5- fluorouracil increased the inhibitory effect on the proliferation of Wi Dr, SW948 and COLO205 in colon cancer cells. With the increase of the concentration of ginsenoside Rg3 (0 M/L, 25 u M/L, 50 u M/L, 75 micron M/L), under the premise of the application of the same concentration of cisplatin or 5- fluorouracil, Wi The proliferation activity of colon cancer cells decreased gradually; 2. the expression of ginsenoside Rg3 in three colon cancer cells was significantly reduced with the increase of ginsenoside Rg3 intervention concentration (0 mu M/L, 25 mu M/L, 50 mu M/L, 75 mu M/L and 100 mu M/L), and the expression of WEE1 was significantly reduced in Wi Dr, SW948 and COLO205 colon cancer cells, and three colon cancer was interfered with 50 micronosides of ginsenoside. Cells, with the increase of ginsenoside Rg3 intervention time (0 h, 6 h, 12 h, 18 h and 24h), the WEE1 expression in Wi Dr, SW948, COLO205 and other colon cancer cells gradually decreased; 3. application of PC plasmid could successfully increase the expression in three colon cancer cells, under the premise of the intervention of the same concentration of cisplatin (10 mu) + ginsenoside (75 mu). With the increase of the transfection concentration of PC DNA-WEE1 plasmids (10 ng, 50 ng, 100 ng, 150 ng), the proliferation activity of Wi Dr, SW948, COLO205 and other colon cancer cells gradually increased. The proliferation activity of colon cancer cells such as 948 and COLO205 increased gradually. Conclusion 1. ginsenoside Rg3 can increase the inhibitory effect of DNA injury drugs (cisplatin and 5- fluorouracil) on the proliferation of colon cancer cells; 2. the inhibitory effect of ginsenoside Rg3 on WEE1 expression is concentration dependent and time dependent; 3. over expression of WEE1 can weaken ginseng soap. The inhibitory effect of glucoside Rg3 sensitized DNA damage drugs (cisplatin and 5- fluorouracil) on the proliferation of colon cancer cells. Second the expression and clinicopathological significance of part WEE1 in colorectal cancer tissue and its clinicopathological significance study on the correlation between the expression of WEE1 protein in colorectal cancer and the clinicopathological parameters and prognosis of colorectal cancer patients. Method 1. in order to investigate the expression of WEE1 in colorectal cancer tissue and para cancer tissue, the expression of WEE1 in fresh colorectal cancer tissues and adjacent tissues was detected by Western blot and Q RT-PCR. 2. in order to clarify the correlation between the expression of WEE1 protein in colorectal cancer tissue and the clinical data of colorectal cancer patients, chi square test analyzed WE. The negative expression and positive expression of E1 protein were related to the age, sex, tumor site, tumor location, tumor diameter, tumor differentiation, lymph node metastasis, distant metastasis, serum CEA level, T stage, N staging, M staging, TNM staging and other clinicopathological parameters; 3. The correlation between the expression of colorectal cancer and the prognosis of colorectal cancer patients. The survival curve was drawn by Kaplan-Meier method. The correlation between the negative expression and positive expression of WEE1 protein and the prognosis of the patients was compared with the Log-rank test. The risk factors affecting the prognosis of the patients with colorectal cancer were analyzed by single factor and multiple factor Cox regression analysis. 1. In 33 cases of colorectal cancer, 18 cases of colorectal cancer tissues, WEE1 protein and m RNA were highly expressed, while 15 cases of colorectal cancer tissues, WEE1 protein and m RNA were low expression; 2. immunohistochemical results showed that in 142 cases of paraffin embedded colorectal cancer tissues, the WEE1 protein was positive in 86 cases. Negative expression was found in 56 cases, and 3.WEE1 positive expression was significantly correlated with tumor differentiation (P=0.033), N staging (P=0.005), TNM staging (P=0.009), Duke 's staging (P=0.001) and lymph node metastasis (P=0.006), and the results were statistically significant. 4. according to the level of WEE1 protein expression, all patients with colorectal cancer were expressed. The average survival time of the WEE1 positive group was significantly shorter than that of the WEE1 negative expression group, and the single factor analysis showed that the tumor size (HR=0.5,95% confidence interval 0.263-0.949, P=0.034), TNM staging (HR=1.402,95% confidence interval 0.934-6.176, P=0.012), M stages (HR=1.562,95% confidence interval 0.231-4.685, HR=1.562,95%) =0.002), liver metastases (HR=3.462,95% confidence interval 1.265-10.256, P=0.014) and WEE1 expression (HR=7.608,95% confidence interval 3.019-19.185, P0.001) are the risk factors affecting the prognosis of colorectal cancer patients. The multifactor Cox proportional risk regression model results show that TNM stages (HR= 2.899,95% confidence interval) and expressions are expressed. 2.93-14.566, P0.001) is an independent risk factor affecting the prognosis of colorectal cancer patients.5. in I patients with colorectal cancer, the expression of WEE1 is not associated with the patients' OS and DFS, but in patients with II and III, WEE1 positive expression suggests that OS and DFS are poor. The positive expression indicates that the prognosis of patients with colorectal cancer is poor. WEE1 positive expression and TNM stage are independent risk factors for prognosis of colorectal cancer.
【学位授予单位】：郑州大学
【学位级别】：博士
【学位授予年份】：2016
【分类号】：R735.35
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