目的:研究羧基末端结合蛋白2(C-terminal binding protein 2,CtBP2)在食管鳞状细胞癌组织中的表达情况及其与食管癌发生发展的关系。方法:Western blot法检测8对食管鳞状细胞癌新鲜冰冻组织、免疫组化法检测90例食管鳞状细胞癌石蜡切片...目的:研究羧基末端结合蛋白2(C-terminal binding protein 2,CtBP2)在食管鳞状细胞癌组织中的表达情况及其与食管癌发生发展的关系。方法:Western blot法检测8对食管鳞状细胞癌新鲜冰冻组织、免疫组化法检测90例食管鳞状细胞癌石蜡切片组织中CtBP2表达情况,结合临床病理和随访资料分析CtBP2表达与患者临床病理参数及总生存率的关系。结果:两法检测结果均显示CtBP2食管鳞状细胞癌组织中的表达明显高于对应的癌旁组织,且CtBP2的表达水平与食管癌的组织学分级(P=0.002)、浸润深度(P=0.032)相关,而与年龄、性别等参数无相关性。Kaplan-Meier分析结果显示,CtBP2高表达组患者的总体生存率明显低于CtBP2低表达组患者。结论:CtBP2在食管鳞状细胞癌组织中表达显著上调,提示其可能与食管鳞状细胞癌的发生发展相关。展开更多
目的探讨SOX2和CTBP1异常表达在非小细胞肺癌(NSCLC)转移中的作用机制。方法 Western blot检测新鲜NSCLC组织及相应的癌旁组织中SOX2和CTBP1蛋白表达;免疫沉淀法分析SOX2和CTBP1在非小细胞肺癌细胞和组织中有无相互作用;用免疫组织化学...目的探讨SOX2和CTBP1异常表达在非小细胞肺癌(NSCLC)转移中的作用机制。方法 Western blot检测新鲜NSCLC组织及相应的癌旁组织中SOX2和CTBP1蛋白表达;免疫沉淀法分析SOX2和CTBP1在非小细胞肺癌细胞和组织中有无相互作用;用免疫组织化学染色法(IHC)检测114例NSCLC石蜡标本中SOX2和CTBP1蛋白表达;通过转染质粒分析SOX2-CTBP1相互作用的调节机制及其对非小细胞肺癌转移的影响。结果 SOX2和CTBP1的表达水平在肺癌组织中要明显高于癌旁组织(P<0.05);SOX2-CTBP1能形成复合物,SOX2、CTBP1在NSCLC转移组中的表达水平明显高于非转移组的表达水平(P<0.05)。CTBP1的高表达与肿瘤分期、组织分化程度﹑SOX2表达、Ki-67表达相关(P<0.05)。在细胞水平,干扰CTBP1表达可下调SOX2及其下游靶基因Snail的表达,从而使H1299细胞体外迁移能力受到抑制。结论 SOX2和CTBP1的异常表达可能与NSCLC发生、发展有关,并且SOX2-CTBP1相互作用可能促进了NSCLC的侵袭转移。展开更多
Stem cell-based therapies have been proposed as a potential treatment for neural regeneration following closed head injury.We previously reported that induced neural stem cells exert beneficial effects on neural regen...Stem cell-based therapies have been proposed as a potential treatment for neural regeneration following closed head injury.We previously reported that induced neural stem cells exert beneficial effects on neural regeneration via cell replacement.However,the neural regeneration efficiency of induced neural stem cells remains limited.In this study,we explored differentially expressed genes and long non-coding RNAs to clarify the mechanism underlying the neurogenesis of induced neural stem cells.We found that H19 was the most downregulated neurogenesis-associated lnc RNA in induced neural stem cells compared with induced pluripotent stem cells.Additionally,we demonstrated that H19 levels in induced neural stem cells were markedly lower than those in induced pluripotent stem cells and were substantially higher than those in induced neural stem cell-derived neurons.We predicted the target genes of H19 and discovered that H19 directly interacts with mi R-325-3p,which directly interacts with Ctbp2 in induced pluripotent stem cells and induced neural stem cells.Silencing H19 or Ctbp2 impaired induced neural stem cell proliferation,and mi R-325-3p suppression restored the effect of H19 inhibition but not the effect of Ctbp2 inhibition.Furthermore,H19 silencing substantially promoted the neural differentiation of induced neural stem cells and did not induce apoptosis of induced neural stem cells.Notably,silencing H19 in induced neural stem cell grafts markedly accelerated the neurological recovery of closed head injury mice.Our results reveal that H19 regulates the neurogenesis of induced neural stem cells.H19 inhibition may promote the neural differentiation of induced neural stem cells,which is closely associated with neurological recovery following closed head injury.展开更多
文摘目的:研究羧基末端结合蛋白2(C-terminal binding protein 2,CtBP2)在食管鳞状细胞癌组织中的表达情况及其与食管癌发生发展的关系。方法:Western blot法检测8对食管鳞状细胞癌新鲜冰冻组织、免疫组化法检测90例食管鳞状细胞癌石蜡切片组织中CtBP2表达情况,结合临床病理和随访资料分析CtBP2表达与患者临床病理参数及总生存率的关系。结果:两法检测结果均显示CtBP2食管鳞状细胞癌组织中的表达明显高于对应的癌旁组织,且CtBP2的表达水平与食管癌的组织学分级(P=0.002)、浸润深度(P=0.032)相关,而与年龄、性别等参数无相关性。Kaplan-Meier分析结果显示,CtBP2高表达组患者的总体生存率明显低于CtBP2低表达组患者。结论:CtBP2在食管鳞状细胞癌组织中表达显著上调,提示其可能与食管鳞状细胞癌的发生发展相关。
文摘目的探讨SOX2和CTBP1异常表达在非小细胞肺癌(NSCLC)转移中的作用机制。方法 Western blot检测新鲜NSCLC组织及相应的癌旁组织中SOX2和CTBP1蛋白表达;免疫沉淀法分析SOX2和CTBP1在非小细胞肺癌细胞和组织中有无相互作用;用免疫组织化学染色法(IHC)检测114例NSCLC石蜡标本中SOX2和CTBP1蛋白表达;通过转染质粒分析SOX2-CTBP1相互作用的调节机制及其对非小细胞肺癌转移的影响。结果 SOX2和CTBP1的表达水平在肺癌组织中要明显高于癌旁组织(P<0.05);SOX2-CTBP1能形成复合物,SOX2、CTBP1在NSCLC转移组中的表达水平明显高于非转移组的表达水平(P<0.05)。CTBP1的高表达与肿瘤分期、组织分化程度﹑SOX2表达、Ki-67表达相关(P<0.05)。在细胞水平,干扰CTBP1表达可下调SOX2及其下游靶基因Snail的表达,从而使H1299细胞体外迁移能力受到抑制。结论 SOX2和CTBP1的异常表达可能与NSCLC发生、发展有关,并且SOX2-CTBP1相互作用可能促进了NSCLC的侵袭转移。
基金supported by the National Natural Science Foundation of China,Nos.82271397(to MG),82001293(to MG),82171355(to RX),81971295(to RX)and 81671189(to RX)。
文摘Stem cell-based therapies have been proposed as a potential treatment for neural regeneration following closed head injury.We previously reported that induced neural stem cells exert beneficial effects on neural regeneration via cell replacement.However,the neural regeneration efficiency of induced neural stem cells remains limited.In this study,we explored differentially expressed genes and long non-coding RNAs to clarify the mechanism underlying the neurogenesis of induced neural stem cells.We found that H19 was the most downregulated neurogenesis-associated lnc RNA in induced neural stem cells compared with induced pluripotent stem cells.Additionally,we demonstrated that H19 levels in induced neural stem cells were markedly lower than those in induced pluripotent stem cells and were substantially higher than those in induced neural stem cell-derived neurons.We predicted the target genes of H19 and discovered that H19 directly interacts with mi R-325-3p,which directly interacts with Ctbp2 in induced pluripotent stem cells and induced neural stem cells.Silencing H19 or Ctbp2 impaired induced neural stem cell proliferation,and mi R-325-3p suppression restored the effect of H19 inhibition but not the effect of Ctbp2 inhibition.Furthermore,H19 silencing substantially promoted the neural differentiation of induced neural stem cells and did not induce apoptosis of induced neural stem cells.Notably,silencing H19 in induced neural stem cell grafts markedly accelerated the neurological recovery of closed head injury mice.Our results reveal that H19 regulates the neurogenesis of induced neural stem cells.H19 inhibition may promote the neural differentiation of induced neural stem cells,which is closely associated with neurological recovery following closed head injury.
