背景与目的所谓肺硬化性血管瘤(so-called pul monary sclerosing hemangioma,PSH)是一种迄今未能确定其组织来源及性质的少见肺部肿瘤,多年来一直是人们研究的热点。本研究通过检测E-cad-herin、β-catenin和p120ctn在PSH表面立方细胞...背景与目的所谓肺硬化性血管瘤(so-called pul monary sclerosing hemangioma,PSH)是一种迄今未能确定其组织来源及性质的少见肺部肿瘤,多年来一直是人们研究的热点。本研究通过检测E-cad-herin、β-catenin和p120ctn在PSH表面立方细胞和间质多角形细胞的免疫表型以探讨其组织来源。方法采用S-P免疫组化法检测25例手术切除PSH标本及8例肺炎性假瘤标本的E-cadherin、β-catenin和p120ctn表达情况。结果25例PSH的立方细胞中,三种上皮粘附分子E-cadherin、β-catenin和p120ctn均呈胞膜强阳性表达,β-catenin在胞膜强阳性表达的同时有胞质表达。而在多角形细胞中,E-cadherin表达缺失,β-catenin胞膜表达缺失伴部分胞质表达,p120ctn胞质表达为主伴少量胞膜表达;三种粘附分子在多角形细胞中的表达存在异质性。血管瘤样区的腔内衬细胞E-cadherin、β-catenin和p120ctn均呈胞质胞膜阳性表达。8例肺炎性假瘤中增生的Ⅱ型肺泡细胞E-cadherin、β-catenin和p120ctn表达与PSH中立方细胞的表达情况相同。结论PSH中的立方细胞可能是增生的Ⅱ型肺泡细胞,而多角形细胞为肿瘤的实质细胞且缺乏分化成熟的上皮细胞所具有的E-cadherin/catenin复合体。血管瘤样区的腔内衬细胞是与立方细胞相同的上皮细胞而非血管内皮细胞。展开更多
AIM:To understand the role of P120ctn in E-cadherin-mediated cell-cell adhesion and signaling as well as inhepatoma cell biological function.METHODS:We stably overexpressed p120ctn isoform3A in BEL-7404 human hepatoma...AIM:To understand the role of P120ctn in E-cadherin-mediated cell-cell adhesion and signaling as well as inhepatoma cell biological function.METHODS:We stably overexpressed p120ctn isoform3A in BEL-7404 human hepatoma cells and studied theeffect of p120ctn on β-catenin and E-cadherin bindingas well as p120ctn and β-catenin subcellular localizationusing immunoprecipitation,Western blotting and confocalmicroscopy.We also investigated the inhibitory effectof p120ctn transfection on the expression of apoptoticprotein survivin survivin and cell cycle regulator cyclin D1in the cells.RERULTS:Western blotting indicated that p120ctnexpression increased after cells were transfected withp120ctn isoform 3A.The protein was located mainlyat membrane under immunofluorescent microscope.β-catenin nuclear expression was reduced afteroverexpression of p120ctn isoform 3A.The p120ctn-E-cadherin binding increased after transfection of p120ctnisoform 3A.Furthermore,overexpression of p120ctndown regulated the expression of apoptotic protein sur-vivin and cell cycle regulator cyclin D1.These effects ledto reduction of cell proliferation.CONCLUSION:Our results indicate that p120ctnplays an important role in regulating the formation ofE-cadherin and-catenin complex,cell apoptosis,cellcycle and cancer cell biological function.展开更多
This study was aimed to investigate the expressions of E-cadherin, p120 ctn, β-catenin and NF-κB in ulcerative colitis（UC） tissues and the implications of their expressions in the pathogenesis of UC. The expressio...This study was aimed to investigate the expressions of E-cadherin, p120 ctn, β-catenin and NF-κB in ulcerative colitis（UC） tissues and the implications of their expressions in the pathogenesis of UC. The expressions of E-cadherin, p120 ctn, β-catenin and NF-κB were detected by immunohistochemistry, and those of p120 ctn and NF-κB by Western blotting in 23 cases of UC and 17 cases of normal colonic tissues. The relationship between the expression of E-cadherin or NF-κB and that of p120 ctn was analyzed by Spearman rank correlation analysis. The results showed that in UC and normal colonic groups, the abnormal expression rate of E-cadherin, p120 ctn, β-catenin, and NF-κB was 52.2% vs. 0（P〈0.05）, 73.9% vs. 23.5%（P〈0.05）, 65.2% vs. 17.6%（P〈0.05） and 78.4% vs. 23.5%（P〈0.05）, respectively. p120 ctn expression was positively correlated with E-cadherin expression（r=0.404, P〈0.05）, but negatively with nuclear NF-κB expression（r= – 0.347, P〈0.05）. Western blotting showed that as compared with the normal controls, the p120 ctn protein level was significantly decreased（P〈0.05）, whereas the NF-κB protein level was increased（P〈0.05） in UC tissues. It was concluded that in the colonic tissues of UC patients, the expressions of E-cadherin, p120 ctn and β-catenin are decreased, suggesting the mucosal barrier is impaired in UC. Moreover, NF-κB is increased and activated in the UC tissues, resulting in the inflammation in UC. p120 ctn may influence the UC development through modulating intercellular adhesion and inflammatory response.展开更多
An important factor in the emergence and progre sion of osteosarcoma(OS)is the dysregulated expression of microRNAs(miRNAs).Transcription factor 7-like 1(TCF7LI),a member of the T cell factor/lymphoid enhancer factor(...An important factor in the emergence and progre sion of osteosarcoma(OS)is the dysregulated expression of microRNAs(miRNAs).Transcription factor 7-like 1(TCF7LI),a member of the T cell factor/lymphoid enhancer factor(TCF/LEF)transcription factor family,interacts with the Wnt signaling pathway regulator β-catenin and acts as a DNA-specific binding protein.This study sought to elucidate the impact of the interaction between miR 3293p and TCF7L1 on.the growth and apoptosis of OS and analyze the regulatory expression relationship between miRNA and mRNA in osteosarcoma cells using a variety of approaches.MiR329-3p was significantly downregulated,while TCF7L1 was considerably up-regulated in all examined OS cell lines.Additionally,a clinical comparison study was performed using the TCGA database.Subsequently,the regulatory relationship between miR-329-3p and TCF7L1 on the proliferation and apoptosis of OS cells was verified through in vitro and in vivo experiments.When miR 329-3p was transfected into the OS cell line,the expression of TCF7L1 decreased,the proliferation of OS cells was inhibited,the cytoskeleton disintegrated,and the nucleus condensed to fom apoptotic bodies.The expression of proteins that indicate apoptosis increased simultaneously.The cell cycle was arrested in the G0/G1 phase,and the G1/S transition was blocked.The introduction of miR 3293p also inhibited downstream Cyclin D1 of the Wnt pathway.Xenograf experiments indicated that the overexpression of miR-329-3p signi ficanly inhibited the growth of OS xenografts in nude mice,and the expression of TCF7L1 and C-Myc in tumor tssues decreased.MiR 329-3p was significantly reduced in OS cells and played a suppressive role in tumorigenesis and proliferation by targeting TCF7L1 both in vitro and in vivo.Osteosarcoma cell cycle arrest and pathway inhibition were observed upon the regulation of TCF7LI by miR 3293p.Summarizing these results,it can be inferred that miR.3293p exerts anticancer efects in osteosarcoma by inhibiting TCF7L1.展开更多
文摘背景与目的所谓肺硬化性血管瘤(so-called pul monary sclerosing hemangioma,PSH)是一种迄今未能确定其组织来源及性质的少见肺部肿瘤,多年来一直是人们研究的热点。本研究通过检测E-cad-herin、β-catenin和p120ctn在PSH表面立方细胞和间质多角形细胞的免疫表型以探讨其组织来源。方法采用S-P免疫组化法检测25例手术切除PSH标本及8例肺炎性假瘤标本的E-cadherin、β-catenin和p120ctn表达情况。结果25例PSH的立方细胞中,三种上皮粘附分子E-cadherin、β-catenin和p120ctn均呈胞膜强阳性表达,β-catenin在胞膜强阳性表达的同时有胞质表达。而在多角形细胞中,E-cadherin表达缺失,β-catenin胞膜表达缺失伴部分胞质表达,p120ctn胞质表达为主伴少量胞膜表达;三种粘附分子在多角形细胞中的表达存在异质性。血管瘤样区的腔内衬细胞E-cadherin、β-catenin和p120ctn均呈胞质胞膜阳性表达。8例肺炎性假瘤中增生的Ⅱ型肺泡细胞E-cadherin、β-catenin和p120ctn表达与PSH中立方细胞的表达情况相同。结论PSH中的立方细胞可能是增生的Ⅱ型肺泡细胞,而多角形细胞为肿瘤的实质细胞且缺乏分化成熟的上皮细胞所具有的E-cadherin/catenin复合体。血管瘤样区的腔内衬细胞是与立方细胞相同的上皮细胞而非血管内皮细胞。
基金Supported by the National Natural Science Foundation of China,No.30160096Natural Science Foundation of Guangxi Zhuang Autonomous Region,No.0007037 and No.0342020
文摘AIM:To understand the role of P120ctn in E-cadherin-mediated cell-cell adhesion and signaling as well as inhepatoma cell biological function.METHODS:We stably overexpressed p120ctn isoform3A in BEL-7404 human hepatoma cells and studied theeffect of p120ctn on β-catenin and E-cadherin bindingas well as p120ctn and β-catenin subcellular localizationusing immunoprecipitation,Western blotting and confocalmicroscopy.We also investigated the inhibitory effectof p120ctn transfection on the expression of apoptoticprotein survivin survivin and cell cycle regulator cyclin D1in the cells.RERULTS:Western blotting indicated that p120ctnexpression increased after cells were transfected withp120ctn isoform 3A.The protein was located mainlyat membrane under immunofluorescent microscope.β-catenin nuclear expression was reduced afteroverexpression of p120ctn isoform 3A.The p120ctn-E-cadherin binding increased after transfection of p120ctnisoform 3A.Furthermore,overexpression of p120ctndown regulated the expression of apoptotic protein sur-vivin and cell cycle regulator cyclin D1.These effects ledto reduction of cell proliferation.CONCLUSION:Our results indicate that p120ctnplays an important role in regulating the formation ofE-cadherin and-catenin complex,cell apoptosis,cellcycle and cancer cell biological function.
基金supported by a grant from the National Natural Science Foundation of China(No.81070009)
文摘This study was aimed to investigate the expressions of E-cadherin, p120 ctn, β-catenin and NF-κB in ulcerative colitis（UC） tissues and the implications of their expressions in the pathogenesis of UC. The expressions of E-cadherin, p120 ctn, β-catenin and NF-κB were detected by immunohistochemistry, and those of p120 ctn and NF-κB by Western blotting in 23 cases of UC and 17 cases of normal colonic tissues. The relationship between the expression of E-cadherin or NF-κB and that of p120 ctn was analyzed by Spearman rank correlation analysis. The results showed that in UC and normal colonic groups, the abnormal expression rate of E-cadherin, p120 ctn, β-catenin, and NF-κB was 52.2% vs. 0（P〈0.05）, 73.9% vs. 23.5%（P〈0.05）, 65.2% vs. 17.6%（P〈0.05） and 78.4% vs. 23.5%（P〈0.05）, respectively. p120 ctn expression was positively correlated with E-cadherin expression（r=0.404, P〈0.05）, but negatively with nuclear NF-κB expression（r= – 0.347, P〈0.05）. Western blotting showed that as compared with the normal controls, the p120 ctn protein level was significantly decreased（P〈0.05）, whereas the NF-κB protein level was increased（P〈0.05） in UC tissues. It was concluded that in the colonic tissues of UC patients, the expressions of E-cadherin, p120 ctn and β-catenin are decreased, suggesting the mucosal barrier is impaired in UC. Moreover, NF-κB is increased and activated in the UC tissues, resulting in the inflammation in UC. p120 ctn may influence the UC development through modulating intercellular adhesion and inflammatory response.
基金The Fund of National Cancer Center Research and Development(26-A-4),The Grants-in-Aid for Scientific Research(Grant Nos.15K10451,16K10866 and 16K20063)from Japan Society for the Promotion of Science.
文摘An important factor in the emergence and progre sion of osteosarcoma(OS)is the dysregulated expression of microRNAs(miRNAs).Transcription factor 7-like 1(TCF7LI),a member of the T cell factor/lymphoid enhancer factor(TCF/LEF)transcription factor family,interacts with the Wnt signaling pathway regulator β-catenin and acts as a DNA-specific binding protein.This study sought to elucidate the impact of the interaction between miR 3293p and TCF7L1 on.the growth and apoptosis of OS and analyze the regulatory expression relationship between miRNA and mRNA in osteosarcoma cells using a variety of approaches.MiR329-3p was significantly downregulated,while TCF7L1 was considerably up-regulated in all examined OS cell lines.Additionally,a clinical comparison study was performed using the TCGA database.Subsequently,the regulatory relationship between miR-329-3p and TCF7L1 on the proliferation and apoptosis of OS cells was verified through in vitro and in vivo experiments.When miR 329-3p was transfected into the OS cell line,the expression of TCF7L1 decreased,the proliferation of OS cells was inhibited,the cytoskeleton disintegrated,and the nucleus condensed to fom apoptotic bodies.The expression of proteins that indicate apoptosis increased simultaneously.The cell cycle was arrested in the G0/G1 phase,and the G1/S transition was blocked.The introduction of miR 3293p also inhibited downstream Cyclin D1 of the Wnt pathway.Xenograf experiments indicated that the overexpression of miR-329-3p signi ficanly inhibited the growth of OS xenografts in nude mice,and the expression of TCF7L1 and C-Myc in tumor tssues decreased.MiR 329-3p was significantly reduced in OS cells and played a suppressive role in tumorigenesis and proliferation by targeting TCF7L1 both in vitro and in vivo.Osteosarcoma cell cycle arrest and pathway inhibition were observed upon the regulation of TCF7LI by miR 3293p.Summarizing these results,it can be inferred that miR.3293p exerts anticancer efects in osteosarcoma by inhibiting TCF7L1.
