目的:探讨生长抑制基因(inhibitor of growth,p33ING1)在结直肠癌中的表达意义,以及p33ING1与结直肠癌临床病理特征的关系及其可能的作用机制。方法:对60例结直肠癌组织及20例癌旁非肿瘤组织标本,应用免疫组化检测肿瘤组织和正常组织的p...目的:探讨生长抑制基因(inhibitor of growth,p33ING1)在结直肠癌中的表达意义,以及p33ING1与结直肠癌临床病理特征的关系及其可能的作用机制。方法:对60例结直肠癌组织及20例癌旁非肿瘤组织标本,应用免疫组化检测肿瘤组织和正常组织的p33ING1、p21WAF1的表达。结果:p33ING1在结直肠癌组织中的表达阳性率为43.3%,在正常组织中为90.0%,显著低于正常组织(P<0.005);p33ING1减低与结直肠癌的Dukes分期及淋巴结转移有一定关系(P<0.005和P<0.01),而与患者的性别、年龄、肿瘤分化程度、肿瘤部位及浸润深度无明显关系(P>0.05)。p33ING1与p21WAF1表达呈正相关关系(P<0.05)。结论:p33ING1在结直肠癌组织中低表达,对结直肠癌的发生、发展可能起着重要的作用;p33ING1、p21WAF1表达可作为判断结直肠癌恶性程度的重要指标之一。展开更多
In order to conduct the fundamental investigation of the effect of 5-FU on HNE1 cells,p33ING1 mRNA level in cellular total RNA was detected quantitatively based on MB assay.During the operation,the effects of 5-FU con...In order to conduct the fundamental investigation of the effect of 5-FU on HNE1 cells,p33ING1 mRNA level in cellular total RNA was detected quantitatively based on MB assay.During the operation,the effects of 5-FU concentrations and treatment time in HNE1 cells and HNE1 cells transfected with p33ING1 were measured in vitro.The results were as follows: p33ING1 mRNA expression level in tumor cells was enhanced not only by the 5-FU concentration but also by lapse of time.The MTT results also proved that high expression of p33ING1 mRNA can increase cell’s sensitivity to chemical drug 5-FU.The detection method based on MB can be used to provide useful evidence quickly and quantitatively for gene expression and new chemical drugs development.展开更多
AIM: To investigate the inhibitory effect of tumor suppressor p33ING1b and its synergy with p53 gene in hepatocellular carcinoma (HCC).METHODS: Recombinant sense and antisense p33ING1b plasmids were transfected into h...AIM: To investigate the inhibitory effect of tumor suppressor p33ING1b and its synergy with p53 gene in hepatocellular carcinoma (HCC).METHODS: Recombinant sense and antisense p33ING1b plasmids were transfected into hepatoma cell line HepG2 with lipofectamine. Apoptosis, G0/G1 arrest, cell growth rate and cloning efficiency in soft agar of HepG2 were analyzed after transfection. In three hepatoma cell lineswith different endogenous p53 gene expressions, the synergistic effect of p33ING1b with p53 was analyzed by flow cytometry and luciferase assay was performed to detect the activation of p53 downstream gene p21WAF1/CIP1. In addition, the expression and mutation rates of p33ING1b in HCC tissues were measured by immunohistochemistry and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP).RESULTS: Overexpression of p33ING1b inhibited cell growth of HepG2, induced more apoptosis and protected cells from growth in soft agar. Combined transfer of p33ING1b and p53 gene promoted hepatoma cell apoptosis, G0/G1 arrest and elevated expression of p21WAF1/CIP1. Immunostaining results showed co-localized P33ING1b with P53 protein in HCC tissues and there was a significant relation between protein expression rates of these two genes (P＜0.01).Among 28 HCC samples, p33ING1b presented a low gene mutation rate (7.1%).CONCLUSION: p33ING1b collaborates with p53 in cell growth inhibition, cell cycle arrest and apoptosis in HCC. Loss or inactivation of p33ING1b normal function may be an important mechanism for the development of HCC retaining wildtype p53.展开更多
文摘目的:探讨生长抑制基因(inhibitor of growth,p33ING1)在结直肠癌中的表达意义,以及p33ING1与结直肠癌临床病理特征的关系及其可能的作用机制。方法:对60例结直肠癌组织及20例癌旁非肿瘤组织标本,应用免疫组化检测肿瘤组织和正常组织的p33ING1、p21WAF1的表达。结果:p33ING1在结直肠癌组织中的表达阳性率为43.3%,在正常组织中为90.0%,显著低于正常组织(P<0.005);p33ING1减低与结直肠癌的Dukes分期及淋巴结转移有一定关系(P<0.005和P<0.01),而与患者的性别、年龄、肿瘤分化程度、肿瘤部位及浸润深度无明显关系(P>0.05)。p33ING1与p21WAF1表达呈正相关关系(P<0.05)。结论:p33ING1在结直肠癌组织中低表达,对结直肠癌的发生、发展可能起着重要的作用;p33ING1、p21WAF1表达可作为判断结直肠癌恶性程度的重要指标之一。
文摘In order to conduct the fundamental investigation of the effect of 5-FU on HNE1 cells,p33ING1 mRNA level in cellular total RNA was detected quantitatively based on MB assay.During the operation,the effects of 5-FU concentrations and treatment time in HNE1 cells and HNE1 cells transfected with p33ING1 were measured in vitro.The results were as follows: p33ING1 mRNA expression level in tumor cells was enhanced not only by the 5-FU concentration but also by lapse of time.The MTT results also proved that high expression of p33ING1 mRNA can increase cell’s sensitivity to chemical drug 5-FU.The detection method based on MB can be used to provide useful evidence quickly and quantitatively for gene expression and new chemical drugs development.
基金Supported by the National Natural Science Foundation of China (Grants No.30070344 and No.30070839)
文摘AIM: To investigate the inhibitory effect of tumor suppressor p33ING1b and its synergy with p53 gene in hepatocellular carcinoma (HCC).METHODS: Recombinant sense and antisense p33ING1b plasmids were transfected into hepatoma cell line HepG2 with lipofectamine. Apoptosis, G0/G1 arrest, cell growth rate and cloning efficiency in soft agar of HepG2 were analyzed after transfection. In three hepatoma cell lineswith different endogenous p53 gene expressions, the synergistic effect of p33ING1b with p53 was analyzed by flow cytometry and luciferase assay was performed to detect the activation of p53 downstream gene p21WAF1/CIP1. In addition, the expression and mutation rates of p33ING1b in HCC tissues were measured by immunohistochemistry and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP).RESULTS: Overexpression of p33ING1b inhibited cell growth of HepG2, induced more apoptosis and protected cells from growth in soft agar. Combined transfer of p33ING1b and p53 gene promoted hepatoma cell apoptosis, G0/G1 arrest and elevated expression of p21WAF1/CIP1. Immunostaining results showed co-localized P33ING1b with P53 protein in HCC tissues and there was a significant relation between protein expression rates of these two genes (P＜0.01).Among 28 HCC samples, p33ING1b presented a low gene mutation rate (7.1%).CONCLUSION: p33ING1b collaborates with p53 in cell growth inhibition, cell cycle arrest and apoptosis in HCC. Loss or inactivation of p33ING1b normal function may be an important mechanism for the development of HCC retaining wildtype p53.
