共查询到20条相似文献,搜索用时 31 毫秒
1.
2.
3.
Jianfei Xue Aidong Zhou Christina Tan Yamei Wu Hsueh-Te Lee Wenliang Li Keping Xie Suyun Huang 《The Journal of biological chemistry》2015,290(30):18662-18670
4.
Xin Zheng Natalia B. Rumie Vittar Xiaohong Gai Maite G. Fernandez-Barrena Catherine D. Moser Chunling Hu Luciana L. Almada Angela L. McCleary-Wheeler Sherine F. Elsawa Anne M. Vrabel Abdirashid M. Shire Andrea Comba Snorri S. Thorgeirsson Youngsoo Kim Qingguang Liu Martin E. Fernandez-Zapico Lewis R. Roberts 《PloS one》2012,7(11)
5.
6.
Andrea Comba Luciana L. Almada Ezequiel J. Tolosa Eriko Iguchi David L. Marks Marianela Vara Messler Renata Silva Maite G. Fernandez-Barrena Elisa Enriquez-Hesles Anne L. Vrabel Bruno Botta Lucia Di Marcotulio Volker Ellenrieder Aldo R. Eynard Maria E. Pasqualini Martin E. Fernandez-Zapico 《The Journal of biological chemistry》2016,291(4):1933-1947
7.
8.
The retinoblastoma protein-interacting zinc finger gene RIZ1 is a putative tumor suppressor gene, and the inactivation of the RIZ1 is frequently found in tumors through a loss of mRNA expression. In order to understand the role of RIZ1 inactivation in the tumorigenesis of hepatocellular carcinoma (HCC), we detected the RIZ1 promoter methylation status in 39 HCCs using a methylation specific PCR (MSP) method, and carried out LOH study with marker P704. We also assessed the associations between the methylation status and clinicopathological parameters, tumor size, tumor differentiation, and fractional allelic loss (FAL). The results showed that the RIZ1 promoter methylated both in advanced tumors (>3 cm), (18/31, 58.0%) and in early tumors (<3 cm), (4/8, 50.0%). There were 54.6% (12/22) tumors with hyper-methylation in the low FAL group and 45.5% (10/22) in the high FAL group. Moreover, the DNA methylation of the RIZ1 promoter was found not only in the poorly differentiated tumors (12/22, 54.6%), but also in the well differentiated tumors (10/22, 45.5%). Among the 22 HCCs (22/39, 56.4%) that showed hyper-methylation at the RIZ1 promoter region, 3 cases showed biallelic methylation. Interestingly, one case showed hyper-methylation on one allele and a loss of heterozygosity (LOH) on the other allele. In other words, 4 HCCs showed the biallelic inactivation of the RIZ1. These results suggest that the inactivation of the RIZ1 by DNA methylation at its promoter region is involved in the tumorigenesis of HCC, particularly in the early stage of disease. 相似文献
9.
10.
11.
Caveolin-1 (Cav-1) has been recently identified to be over-expressed in hepatocellular carcinoma (HCC) and promote HCC cell motility and invasion ability via inducing epithelial-mesenchymal transition (EMT). However, the mechanism of aberrant overexpression of Cav-1 remains vague. Here, we observed that Cav-1 expression was positively associated with GLI1 expression in HCC tissues. Forced expression of GLI1 up-regulated Cav-1 in Huh7 cells, while knockdown of GLI1 decreased expression of Cav-1 in SNU449 cells. Additionally, silencing Cav-1 abolished GLI1-induced EMT of Huh7 cells. The correlation between GLI1 and Cav-1 was confirmed in tumor specimens from HCC patients and Cav-1 was found to be associated with poor prognosis after hepatic resection. The relationship between protein expression of GLI1 and Cav-1 was also established in HCC xenografts of nude mice. These results suggest that GLI1 may be attributed to Cav-1 up-regulation which plays an important role in GLI1-driven EMT phenotype in HCC. 相似文献
12.
13.
14.
A multipotent progenitor domain guides pancreatic organogenesis 总被引:3,自引:0,他引:3
15.
Ikuo Nakamura Maite G. Fernandez-Barrena Maria C. Ortiz-Ruiz Luciana L. Almada Chunling Hu Sherine F. Elsawa Lisa D. Mills Paola A. Romecin Kadra H. Gulaid Catherine D. Moser Jing-Jing Han Anne Vrabel Eric A. Hanse Nicholas A. Akogyeram Jeffrey H. Albrecht Satdarshan P. S. Monga Schuyler O. Sanderson Jesus Prieto Lewis R. Roberts Martin E. Fernandez-Zapico 《The Journal of biological chemistry》2013,288(29):21389-21398
16.
Pierrat MJ Marsaud V Mauviel A Javelaud D 《The Journal of biological chemistry》2012,287(22):17996-18004
17.
18.
19.
20.
Kanato K Hosen N Yanagihara M Nakagata N Shirakata T Nakazawa T Nishida S Tsuboi A Kawakami M Masuda T Oka Y Oji Y Ijpenberg A Hastie ND Sugiyama H 《Biochemical and biophysical research communications》2005,326(4):836-843
It is well known that the Wilms' tumor gene WT1 plays an important role in cell proliferation and differentiation, and in organ development. In this study, to examine the role of the WT1 gene in lineage determination, fetal liver cells from LacZ-transgenic mice, in which WT1 expression was marked by the expression of the LacZ gene driven by WT1 promoter, were FACS-sorted according to LacZ expression of high (LacZ(++)) or undetectable (LacZ(-)) levels, which paralleled endogenous WT1 expression levels. LacZ(++) fetal liver cells were enriched by hepatocyte and endothelial progenitor cells. These results indicated that WT1 expression is a common marker of both hepatocyte and endothelial progenitors. These results also implied a role of the WT1 gene in lineage determination. 相似文献