目的 检测分化抑制因子1（Id-1）在肝细胞肝癌组织中和正常肝组织中的表达情况，了解Id-1与肝细胞肝癌患者预后关系。 方法 对获得的19例肝细胞肝癌组织标本和8例正常肝组织进行免疫组织化学染色，并对染色结果进行分级。借助SPSS软件，分析肝细胞肝癌组织标本与正常肝组织标本中的Id-1表达强度区别，Id-1与甲胎蛋白（AFP）相关性，及Id-1表达强度与肝癌患者预后之间的关系。 结果 免疫组织化学染色结果显示所有标本均表达为阳性，其中3例（+），7例（++），10例（+++）7例（++++），肝细胞肝癌组织标本与正常肝组织标本差异有统计学意义（P＜0.05）；Id-1表达与血液中AFP水平相关不显著（r=−0.121，P=0.621）；Spearman等级相关分析显示患者生存时间与Id-1表达呈负相关（r=−0.567，P=0.011）。 结论 Id-1在肝癌组织中表达增高 ，Id-1表达水平与生存时间呈负相关，但和AFP无明显相关。
Objectives To investigate the expressions and significance of E2F1, ID1, and Bax protein in gallbladder adenocarcinoma tissues. MethodsThe expressions of E2F1, ID1, and Bax protein in 70 cases of gallbladder adenocarcinoma, 20 cases of high level intraepithelial neoplasia, 30 cases of low level intraepithelial neoplasia, and 20 cases of cholecystitis tissues were tested by using immunohistochemical method. ResultsThe positive expression rates of E2F1, ID1, and Bax protein in gallbladder adenocarcinoma was 84.3%, 70.0%, and 25.7%, respectively; the positive expression rates in high level intraepithelial neoplasia was 75.0%, 65.0%, and 55.0%, respectively; the positive expression rates in low level intraepithelial neoplasia was 16.7%, 23.3%, and 56.7%, respectively; and the positive expression rates in cholecystitis tissues was 10.0%, 20.0%, and 75%, respectively.The positive expression rates of E2F1 and ID1 protein in gallbladder adenocarcinoma were significantly higher than those intraepithelial neoplasia and cholecystitis tissues (P < 0.05), but the positive expression rate of Bax protein in gallbladder adenocarcinoma was lower (P < 0.05).The expressions of E2F1 and ID1 protein were significantly correlated with clinical Nevin staging of gallbladder adenocarcinoma (P < 0.05), but not correlated with the gallbladder adenocarcinoma differentiation degree (P > 0.05).The expression of Bax protein was related to the gallbladder adenocarcinoma differentiation degree (P < 0.05), but not correlated with clinical Nevin staging (P > 0.05).The expression of E2F1 protein was negatively correlated with expression of Bax protein (r=-0.375, P < 0.05), ID1 protein expression has nothing to do with the protein expression of Bax protein (P > 0.05).The expression of E2F1 protein was positively correlated with ID1 protein (r=7.031, P < 0.05). ConclusionsThe E2F1, ID1, and Bax may play an important role in the generation and development of the gallbladder adenocarcinoma.The combined detection of E2F1, ID1, and Bax have important guiding significance for auxiliary diagnosis and clinical staging of gallbladder adenocarcinoma.
ObjectiveTo study the effect of inhibitor of differentiation 1 (Id1) gene transfection on bone morphogenetic protein 2 (BMP-2) promoting the expressions of collagen type Ⅱ (COL Ⅱ) and aggrecan (ACAN) in intervertebral cartilage endplate cells (EPCs). MethodsEPCs were harvested from the New Zealand white rabbits, the 2nd generation EPCs were used for experiment. The transfection efficiency of green fluorescent protein blank lentivirus, high expression of Id1 lentivirus, RNA interference (RNAi) Id1 lentivirus transfection in the EPCs were observed by the fluorescence microscopy, real-time fluorescence quantitative PCR, and Western blot. Blank vector, single BMP-2 gene, BMP-2 and Id1 genes were transfected into EPCs, respectively. The cell morphology and the expressions of COL Ⅱ and ACAN in each group were observed. ResultsLentiviral transfection had no significant effect on the cell morphology. The EPCs were effectively transfected by the high expression Id1 lentivirus and RNAi Id1 lentivirus; the expression of Id1 mRNA was also significantly interfered. The expressions of COL Ⅱ and ACAN mRNA and synthesis of COL Ⅱ and ACAN protein were significantly higher in BMP-2 lentivirus and high expression Id1 lentivirus groups than control group (P<0.05). The expression of COL Ⅱ and ACAN protein were down regulated in the cartilage endplate cells when the expression of Id1 gene was decreased (P<0.05). ConclusionUp-regulation of Id1 gene expression can enhance the effects of BMP-2 on the synthesis of COL Ⅱ and ACAN in EPCs.