5 results on '"Wen-Yue Zhuang"'
Search Results
2. [Effect of AML1-ETO fusion protein on the expression of BCL-2]
- Author
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Wen-Yue, Zhuang, Zheng-Yi, Li, Yun, Zhao, Jian-Nong, Cen, Wen-Zhuo, Zhuang, and Zi-Xing, Chen
- Subjects
Leukemia, Myeloid, Acute ,RUNX1 Translocation Partner 1 Protein ,Oncogene Proteins, Fusion ,Proto-Oncogene Proteins c-bcl-2 ,Gene Expression Regulation, Leukemic ,Core Binding Factor Alpha 2 Subunit ,Humans ,U937 Cells - Abstract
This study was aimed to investigate the effect of AML1-ETO fusion protein on the anti-apoptotic gene BCL-2 in leukemic cells and to explore its role in leukemogenesis. The apoptotic levels of U937-WT, U937-Mock and U937-A/E1-4 cells were examined by flow cytometry. And cleaved caspase-3 protein expression was detected by Western blot. BCL-2 gene expression both in AML1-ETO-expressing cells or U937 nonexpressing cells and in leukemia cells of AML patients with or without t(8;21) was assessed by quantitative PCR. The chromatin immunoprecipitation (ChIP)-based PCR was used to investigate the direct interaction between the AML1-ETO and BCL-2 promoter in AML1-ETO positive leukemia cell line. The results indicated that in U937-A/E cells but not in U937-WT or U937-Mock cells, apoptotic cells statistically significantly increased, and AML1-ETO expression also significantly enhanced activation of caspase-3. AML1-ETO-expressing cell subclones displayed significantly low levels of BCL-2 mRNA in comparison with the non-transfected U937. In primary bone marrow cells of acute myeloid leukemia containing AML1-ETO, levels of BCL-2 mRNA were markedly lower as compared with other acute myeloid leukemias lacking this translocation. The enriched regions in transfected cells were located within BCL-2 promoter. It is concluded that BCL-2 is the direct target gene of AML1-ETO. AML1-ETO can down-regulate the expression of BCL-2.
- Published
- 2013
3. Epigenetic silencing of Bcl-2, CEBPA and p14(ARF) by the AML1-ETO oncoprotein contributing to growth arrest and differentiation block in the U937 cell line
- Author
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Jiannong Cen, Zi-Xing Chen, Wen-Yue Zhuang, and Yun Zhao
- Subjects
Cancer Research ,Chromatin Immunoprecipitation ,Oncogene Proteins, Fusion ,Leukemia, Myelomonocytic, Acute ,Histone H3 ,RUNX1 Translocation Partner 1 Protein ,hemic and lymphatic diseases ,Cell Line, Tumor ,CEBPA ,Tumor Suppressor Protein p14ARF ,Humans ,neoplasms ,Transcription factor ,Regulator gene ,Cell Proliferation ,biology ,Promoter ,Cell Differentiation ,General Medicine ,U937 Cells ,Molecular biology ,Chromatin ,DNA-Binding Proteins ,Gene Expression Regulation, Neoplastic ,Histone ,Oncology ,Proto-Oncogene Proteins c-bcl-2 ,Core Binding Factor Alpha 2 Subunit ,biology.protein ,CCAAT-Enhancer-Binding Proteins ,Chromatin immunoprecipitation - Abstract
The AML1-ETO fusion transcription factor generated by the t(8;21) translocation is considered to deregulate the expression of genes that are crucial for normal differentiation and proliferation of hematopoietic progenitors, resulting in acute myelogenous leukemia by recruiting co-repressor complexes to DNA. To investigate the role of AML1-ETO in leukemogenesis, we transfected the cloned AML1-ETO cDNA and expressed the AML1-ETO protein in U937 myelomonocytic leukemia cells. By focusing on the anti-apoptotic gene Bcl-2, the key regulator gene of granulocytic differentiation CCAAT/enhancer-binding protein α (CEBPA) and the tumor suppressor gene p14(ARF), we found that both AML1-ETO-expressing cell lines and t(8;21) leukemia samples displayed low levels of these three genes. Chromatin immunoprecipitation assays demonstrated that Bcl-2, CEBPA and p14(ARF) were direct transcriptional targets of AML1-ETO. The universal binding of AML1-ETO to genomic DNA resulted in recruitment of methyl-CpG binding protein 2 (MeCP2), reduction of histone H3 or H4 acetylation and increased trimethylation of histone H3 lysine 9 as well as lysine 27 indicating that AML1-ETO induced heterochromatic silencing of Bcl-2, CEBPA and p14(ARF). These results suggested that the aberrant transcription factor AML1-ETO epigenetically silenced the function of the Bcl-2, CEBPA and p14(ARF) genes by inducing repressed chromatin configurations at their promoters through histone modifications.
- Published
- 2013
4. Schisandra polysaccharide inhibits hepatic lipid accumulation by downregulating expression of SREBPs in NAFLD mice.
- Author
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Chun-Mei Wang, Rong-Shuang Yuan, Wen-Yue Zhuang, Jing-Hui Sun, Jin-Ying Wu, He Li, and Jian-Guang Chen
- Subjects
SCHISANDRA chinensis ,POLYSACCHARIDES ,FATTY liver ,STEROL regulatory element-binding proteins ,ANIMAL models in research - Abstract
Background: Hepatoprotective effects of Chinese herbal medicine Schisandra Chinensis (Schisandra) have been widely investigated. However, most studies were focused on its lignan extracts. We investigated the effects of Schisandra polysaccharide (SCP) in a mouse model of non-alcoholic fatty liver disease (NAFLD), and studied its effect on sterol regulatory element binding proteins (SREBPs) and the related genes. Methods: The mouse model of NAFLD was established by feeding mice with a high-fat diet for 16 weeks. Effect of SCP-treatment (100 mg/kg, once daily for 12 weeks) on biochemical parameters and liver histopathology was assessed. Relative levels of sterol regulatory element-binding proteins (SREBPs) and their gene expressions were determined by quantitative real-time polymerase chain reaction and Western Blot. Results: SCP significantly reduced the liver index by 12.0%. Serum levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol, alanine aminotransferase and aspartate aminotransferase were decreased by 31.3, 28.3, 42.8, 20.1 and 15.5%, respectively. Serum high-density lipoprotein cholesterol was increased by 26.9%. Further, SCP lowered hepatic TC and TG content by 27.0% and 28.3%, respectively, and alleviated fatty degeneration and necrosis of liver cells. A significant downregulation of mRNA and protein expressions of hepatic lipogenesis genes, SREBP-1c, fatty acid synthase and acetyl-CoA carboxylase, and the mRNA expression of liver X receptor α (LXRα) was observed in NAFLD mice treated with SCP. SCP also significantly reduced the hepatic expression of SREBP-2 and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). Conclusion: These findings demonstrate the hepatoprotective effects of SCP in a mouse model of NAFLD; the effects may be mediated via downregulation of LXRα/SREBP-1c/FAS/ACC and SREBP-2/HMGCR signaling pathways in the liver. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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5. Epigenetic Silencing of Bcl-2, C/Ebpa and p14ARF by the AML1/ETO Oncoprotein Contributing to Growth Arrest and Differentiation Blockage
- Author
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Zi-Xing Chen and Wen-yue Zhuang
- Subjects
Tumor suppressor gene ,Immunology ,Promoter ,Cell Biology ,Hematology ,Transfection ,Biology ,Biochemistry ,Molecular biology ,Chromatin ,Histone H3 ,chemistry.chemical_compound ,RUNX1 ,chemistry ,p14arf ,hemic and lymphatic diseases ,Transcription factor - Abstract
Abstract 3617 The t(8; 21) is one of the most frequent chromosomal translocations associated with acute leukemia. The AML1(RUNX1)-ETO(MTG8) fusion transcription factor generated by the t (8; 21) translocation is believed to deregulate the expression of genes that are crucial for normal differentiation and proliferation of hematopoietic progenitors, resulting in acute myelogenous leukemia by recruiting co-repressor complexes to DNA. To investigate the role of AML1-ETO in leukemogenesis, we transfected the cloned AML1-ETO cDNA with plasmid and expressed the AML1-ETO protein in U937 myelomonocytic leukemia cells. Interestingly, we found dichotomous phenomena in these transfected leukemic cells, i.e. growth arrest versus differentiation block (detailed data?). The AML1-ETO transfected U937cells were growing significantly slower than that of empty vector-transfected cells and nontransfected cells (P Disclosures: No relevant conflicts of interest to declare.
- Published
- 2010
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