演讲嘉宾--张华凤

张华凤
hzhang22@ustc.edu.cn
http://biox.ustc.edu.cn/szdw/js/201006/t20100630_23329.html
中国科学技术大学生命科学学院教授、 中组部“青年千人计划” 中科院“百人计划”入选者、 国家“杰出青年科学基金”获得者
研究学习经历:

在日本的东京大学、美国的国立癌症研究所(NCI/NIH)、约翰霍普金斯大学医学院以及中国科学技术大学从事肿瘤学的研究,致力于解析肿瘤代谢异常和肿瘤微环境因素的相互关系及抗肿瘤药物的研发,研究成果发表于Cancer Cell, PNAS, Nature Communications, Cell Reports, Cell Research, Angew Chem Int Ed Engl. 等期刊上,这些工作系统地揭示了在肿瘤微环境中,肿瘤细胞如何适应低氧、营养匮乏等应激状态而生存并通过代谢改变等来促进肿瘤的增殖和发展,产生了较为广泛的影响。

近期发表论文:
  1. Huang D#, Li T#, Wang L, Zhang L, Yan R, Kui Li, Xing S, Wu G, Hu L, Jia W, Lin S, Dang CV, Song L*, Gao P*, Zhang H* Hepatocellular carcinoma redirects to ketolysis for progression under nutrition stress. Cell Research 2016,In Press.
  2. Ma X, Li C, Sun L, Huang D, Li T, He X, Wu G, Yang Z, Zhong X, Song L, Gao P*, Zhang H* Lin28/let-7 axis regulates aerobic glycolysis and cancer progression via PDK1.Nature Communications 2014 Oct 10;5:5212.
  3. Sun L, Song L, Wan Q, Wu G, Li X, Wang Y, Wang J, Liu Z, Zhong X, He X, Shen S, Wang Y, Gao P*, Tang H*, Zhang H*  cMyc-Mediated Activation of Serine Biosynthesis Pathway is Critical for Cancer Progression under Nutrient Deprivation  Conditions. Cell Research 2015 Apr;25(4):429-44
  4. Yuan Y, Wang L, Du W, Ding Z, Zhang J, Han T, An L, Zhang H*, Liang G*. Intracellular Self-Assembly of Taxol Nanoparticles for Overcoming Multidrug Resistance. Angew Chem Int Ed Engl. 2015 Aug 10;54(33):9700-4
  5. Huang D, Li T, Li X, Zhang L, Sun L, He X, Zhong X, Jia D, Song L, Semenza GL, Gao P and Zhang H* HIF-1-Mediated Suppression of Acyl-CoA Dehydrogenases and Fatty Acid Oxidation is Critical for Cancer Progression. Cell Reports 2014 Sep 25;8(6):1930-42.
会议报告摘要:
Hepatocellular carcinoma redirects to ketolysis for progression under nutrition stress(4月22日 16:50-17:20pm)

Cancer cells rewire metabolic pathways to obtain sufficient energy or building blocks to support rapid cell growth and proliferation . Hypoxia and nutrition deprivation are central characterictics of tumor microenvironment. In this presentation, I will discuss our recent findings that, while cancer cells are known to consume glucose, glutamine and fatty acids for energy as well as carbon and nitrogen sources for anabolism, under nutrition deprivation conditions, they also reprogram their metabolic pathways by seeking alternative nutrient sources to meet the demands for proliferation. Specifically, we discovered that catabolism of ketone bodies, which are produced in the liver but not consumed by normal adult liver cells, is re-activated in hepatocellular carcinoma (HCC) cells under nutrition deprivation conditions. Mechanistically, 3-oxoacid-CoA transferase enzyme (OXCT1), a rate-limiting ketolytic enzyme whose expression is suppressed in normal adult liver tissues, is re-induced for energy production under nutrition deprivation conditions in HCC cells. Analysis of clinical HCC samples reveals that increased OXCT1 expression predicts higher patient mortality. Taken together, we uncover here a novel metabolic adaptation by which nutrition-stressed HCC cells employ ketone bodies for cancer progr.

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第四届肿瘤基础和转化医学前沿国际研讨会