黄灿华
1)功能基因组学与蛋白质组学研究;2)病毒与宿主相互作用机理;3)表观遗传学与表观基因治疗
个性化签名
- 姓名:黄灿华
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学术头衔:
博士生导师, 教育部“新世纪优秀人才支持计划”入选者
- 职称:-
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学科领域:
生物化学
- 研究兴趣:1)功能基因组学与蛋白质组学研究;2)病毒与宿主相互作用机理;3)表观遗传学与表观基因治疗
黄灿华 教授,博士生导师。2000年在中国科学院获博士学位, 随后在新加坡国立大学生物系作博士后研究。2003 年8 月被新加坡国立大学肿瘤研究所聘为Research Scientist。2005年9月回国任四川大学生物治疗国家重点实验室教授,蛋白质组学科带头人。2007年获教育部“新世纪优秀人才计划”资助。美国生物化学与分子生物学会(ASBMB)会员(2008-)先后承担科技部863和国家自然科学基金等课题。回国五年来作为通讯作者在Mol Cell Proteomics、Autophagy、 Proteomics、 J Proteome Res、Mol Cancer、Int J Cancer、Biochem Pharmacol等杂志上发表SCI论文20篇;协助培养出两篇“全国百篇优秀博士论文(2009)”。应邀在Expert Rev Proteomics、Comb Chem High Throughput Screen、Science in China等国际学术上发表系统生物学与高通量药物靶标筛选前沿综述。现为Mol Cell Proteomics、Proteomics、J Proteome Res、 Biochem Pharmacol、J Pharmacol Exp Ther等国际学术刊物特邀审稿人.
研究方向
1)功能基因组学与蛋白质组学研究;2)病毒与宿主相互作用机理;3)表观遗传学与表观基因治疗
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主页访问
1975
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关注数
0
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成果阅读
190
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成果数
5
黄灿华, Zhengyu Li, Xia Zhao‡, Shujun Bai, Zhi Wang, Lijuan Chen, Yuquan Wei, and Canhua Huang§
Molecular & Cellular Proteomics 7: 1810-1823, 2008.,-0001,():
-1年11月30日
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黄灿华, Aiping Tong, † Lantu Gou, † Quek Choon Lau, ‡ Bin Chen, † Xia Zhao, † Jiong Li, † Hong Tang, † Lijuan Chen, † Minghai Tang, † Canhua Huang, *, † and Yu-quan Wei*, †
Journal of Proteome Research 2009, 8, 1037-1046,-0001,():
-1年11月30日
The hepatitis B virus-encoded X (HBx) protein coactivates transcription of a variety of viral and cellular genes and it is believed to play essential roles in viral replication and hepatocarcinogenesis. To examine the pleiotropic effects of HBx protein on host cell protein expression, we utilized 2-DE and MS analysis to compare and identify differentially expressed proteins between a stable HBx-transfected cell line (HepG2-HBx), constitutively expressing HBx, and vector control cells. Of the 60 spots identified as differentially expressed (over 2-fold, p<0.05) between the two cell lines, 54 spots were positively identified by MS/MS analysis. Several recent studies suggested that HBx was involved in regional hypermethylation of tumor suppressor genes and global hypomethylation of satellite 2 repeats during hepatocarcinogenesis; however, no specific gene has been reported as hypomethylated by HBx.Promoter methylation analysis was examined for those protein spots showing significant alterations, and our results revealed that specific genes, such as aldehyde dehydrogenase 1 (ALDH1), can be hypomethylated by HBx, and two calcium ion-binding proteins, S100A6 and S100A4, were hypermethylated by HBx and could be re-expressed by AZA (DNA methylase inhibitor) treatment. Moreover, via cluster and pathway analysis, we proposed a hypothetical model for the HBx regulatory circuit involving aberrant methylation of retinol metabolism-related genes and calcium homeostasis-related genes. In summary, we profiled proteome alterations between HepG2-HBx and control cells, and found that HBx not only induces regional hypermethylation but also specific hypomethylation of host cell genes.
HBx • HBV • hepatocellular carcinoma • proteomics • two-dimensional gel electrophoresis
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黄灿华, Zhengyu Li, , Canhua Huang*, Shujun Bai, Xiaoling Pan, Rong Zhou, Yuquan Wei and Xia Zhao*
Int. J. Cancer: 123, 2377-2383 (2008),-0001,():
-1年11月30日
With the aim to translate the discovery from proteomic research into clinical applications, we identified epidermal fatty acid-binding protein (E-FABP) and calcyphosine (CAPS) by MALDI-QTOF MS and validated their overexpressions by immunoblotting. Their expression statuses were examined by immunohistochemistry in 39 normal endometrium, 29 endometrial intraepithelial neoplasia (EIN) and 84 endometrial cancer (EC) cases. We evaluated the correlations to the clinicopathologic characteristics and determined whether these proteins had prognostic significance. Expressions of E-FABP and CAPS were increased 2.64- and 2.18-fold in EC by immunoblotting. Immunoreactivity of both E-FABP and CAPS were stronger in EC than in EIN or normal tissues (p<0.001 and <0.001). Stronger mmunoreactivity of E-FABP and CAPS were shown to present with poor differentiation (p5 0.032 and 0.001), but no elevance was observed with staging (p 5 1.368and 4.306). Survival analysis indicated that mmunoreactivity of CAPS was correlated to poor survival (p 5 0.018), but E-FABP status appeared to be no correlation to the clinical outcome of patients (p 5 0.865). Multivariate analysis indicated that CAPS might be an independent prognostic factor for survival in patients with EC (p 5 0.008). Results demonstrated the ubiquitous overexpressions of E-FABP and CAPS in EC and the correlations to the clinicopathologic parameters. CAPS might be a potential prognostic factor for survival in patients with EC. The research pattern from proteomics to clinical specimens would have widespread applications.
E-FABP, CAPS, endometrial cancer, prognostic factor, survival analysis
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黄灿华, Jun Shen a, c, , Canhua Huang b, Lu Jiang a, Feng Gao a, Zhi Wanga, Yuanyuan Zhang a, Jingping Bai a, Hongmei Zhou a, Qianming Chen a, *
biochemical pharma cology73(2007)1901-1909,-0001,():
-1年11月30日
Both the resistance of tumor cells to cisplatin and dose-related toxicity remain two of the most important problems in the chemotherapy of clinical oral squamous cell carcinoma (OSCC). Researchers have been seeking a combinative treatment regimen to improve the effect of chemotherapy. As potent new anti-cancer drugs, histone deacetylase inhibitors (HDACIS) have been reported to be associated with chromatin modification and display synergistic activities with some traditional chemotherapeutic agents. In this study, we evaluated the potential combinative effect of low dose cisplatin and suberoylanilide hydroxamic acid (SAHA, one of the most potent HDACIS) in OSCC cell lines. Cell viability and apoptotic assay were examined. Compared with either cisplatin (4mg/ml) or SAHA (2mM) treated alone, co-administration of both drugs synergistically induces cytotoxicity and apoptosis in both Tca8113 and KB cell lines. Furthermore, diverse apoptosis-associated proteins, including p53, BID, cytochrome C and caspase-3 were involved in the induction of apoptosis. Our results suggest that concurrent treatment with SAHA enhances tumor cell sensitivity to subtoxic doses of cisplatin. This may be regarded as a novel strategy for treatment of OSCC.
Cisplatin, Suberoylanilide hydroxamic acid, Apoptosis, Chemotherapy, Oral squamous cell carcinoma
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黄灿华, Canhua Huang a, Hiroshi Ida b, Kosei Ito a, b, Haiyuan Zhang a, Yoshiaki Ito a, *
biochemical pharmacology73(2007)990-1000,-0001,():
-1年11月30日
Vorinostat (suberoylanilide hydroxamic acid, SAHA) represents a new class of highly potent histone deacetylase (HDAC) inhibitors that cause growth arrest, differentiation, and apoptosis of many tumor types in vitro and in vivo. RUNX3, a gastric tumor suppressor, is epigenetically silenced in gastric cancer cells. This study investigates the role of RUNX3 in vorinostat-induced suppression of gastric cancer cell growth. RUNX3 was up-regulated by vorinostat in gastric cancer cell lines not expressing RUNX3. In terms of cell viability, the mean IC50 of vorinostat in RUNX3-negative cells was significantly lower than that seen in RUNX3-positive cells, indicating that the former are more sensitive to vorinostat in terms of growth arrest than are RUNX3-positive lines. The mechanism underlying this difference was found to be reactivation of RUNX3 expression by vorinostat and concomitant increase in acetylated histone H3 in the promoter region of RUNX3. Using three RUNX3-negative cell lines, we determined the contribution of RUNX3 reactivation to growth inhibition and induction of apoptosis following treatment of cells with vorinostat and found that upregulated RUNX3 was significantly responsible for tumor suppressive activities.
Vorinostat, RUNX3, Gastric cancer, Chemotherapy
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