吴兴中
生物分子结构与功能和细胞信号转导领域的研究;肿瘤糖结构与功能,肿瘤转移侵袭机制的研究。
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- 姓名:吴兴中
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学术头衔:
博士生导师
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学科领域:
生物化学
- 研究兴趣:生物分子结构与功能和细胞信号转导领域的研究;肿瘤糖结构与功能,肿瘤转移侵袭机制的研究。
吴兴中教授,博士生导师。1982年毕业于浙江医科大学获学士学位, 1988年毕业于上海第二医科大学研究生。1997年去美国NIH癌症研究所进修,2000年日本大阪大学医学院生物化学系做访问研究员,2002香港大学医学院学习。
研究方向:生物分子结构与功能和细胞信号转导领域的研究;肿瘤糖结构与功能,肿瘤转移侵袭机制的研究。
主持国家自然科学基金3项,上海市教委重点学科项目1项。以第一作者身份发表学术论文34篇。曾获得部级科技进步奖三项。此外,长期从事临床医学5年制、7年制生物化学教学,八年制,基地班和夜大学的教学,作为七年制 /基地班 /八年制学生导师,带教基地班实习生。承担硕士生高级生化教学,博士生医学分子生物学的教学工作。1999年获得上海市育才奖。主编《正常人体形态与功能学I》等教材。
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吴兴中, Bi-Zhi Shi a, Ping Hu a, Fei Geng a, Pei-Jie He b, Xing-Zhong Wu a, *
Biochemical and Biophysical Research Communications 332(2005)934-940,-0001,():
-1年11月30日
In this study, significantly higher expression of Gal3ST-2 (Gal: 3-O sulfotransferase-2) and 30-sulfated glycoconjugates were observed in highly metastastic cancer cells and in larynx cancer tissues with lymph node metastasis than those in lowly metastatic cancer cells and larynx cancer tissues without metastasis (P<0.01, n=42). These results indicated that there was a marked correlation between the expression of Gal3ST-2 and tumor metastasis potential. After RNAi transfection, a striking morphological change of SMMC7721 hepatoma cells from polygon to shuttle shape and significant decrease in adhesion to sL-selectin and HUVEC were observed. Interestingly, the expression of integrin subunit aV was markedly downregulated and 30-sulfated subunit aV almost disappeared in the transfectants, but integrin subunit b3 almost had no change. These results suggested that Gal3ST-2 was involved in tumor metastasis process by regulation of adhesion ability to selectins and expression of integrins.
Gal3ST-2, Sulfated glycan, Tumor metastasis
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吴兴中, Fei GENG, Bi Zhi SHI, Yun Feng YUAN, Xing Zhong WU*
Cell Research (2004); 14(5):423-433,-0001,():
-1年11月30日
It is well documented that the glycosylation of E-cadherin is correlated with cancer metastasis, but whether Ecadherin could be core fucosylated remains largely unknown. We found that E-cadherin was core fucosylated in highly metastatic lung cancer cells while absent in lowly metastatic lung cancer cells. Since α-1,6 Fucosyltransferase (α-1,6 FucT) is known to catalyze the reaction of core fucosylation, we investigated the biological function of core fucosylation on E-cadherin by α-1,6 FucT targeted RNAi and transfecting α-1,6 FucT expression vector. As a result, calcium dependent cell-cell adhesion mediated by E-cadherin was strengthened with the reduction of core fucosylation on Ecadherin after RNAi and was weakened with the elevated core fucosylation on E-cadherin after α-1,6 FucT over expression. Our data indicated that α-1,6 FucT could regulate E-cadherin mediated cell adhesion and thus play an important role in cancer development and progression. Computer modeling showed that core fucosylation on E-cadherin could significantly impair three-dimensional conformation of N-glycan on E-cadherin and produce conformational asymmetry so as to suppress the function of E-cadherin. Furthermore, the relationship between the expression of core fucosylated E-cadherin and clinicopathological background of lung cancer patients was explored in lung cancer tissue of patients. It turns out to demonstrate that core fucosylated E-cadherin could serve as a promising prognostic indicator for lung cancer patients.
Core fucosylated E-cadherin,, prognosis,, cancer metastasis,, RNA interference,, molecular modeling.,
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