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李兵輝,，博士，教授,，PI,，博士生導(dǎo)師
教育背景
2001.09~2006.04理學(xué)博士,，中國(guó)科學(xué)院研究生院,。專業(yè)：生物化學(xué)與分子生物學(xué)。
1996.09~2000.07理學(xué)學(xué)士,，江西南昌大學(xué)。專業(yè)：生物工程,。
工作經(jīng)歷
2007.11~2010.10研究助理(Research Professional Associate)，芝加哥大學(xué),。從事癌癥與能量代謝方面的研究,。
2010.12~至今教授，天津醫(yī)科大學(xué)附屬腫瘤醫(yī)院腫瘤研究所,。
研究興趣
本課題組將著重闡述代謝酶,、代謝產(chǎn)物及癌細(xì)胞命運(yùn)之間的關(guān)系，以尋找新穎的,、特異的抗癌靶點(diǎn)為主要任務(wù),！我們的研究興趣在：
1、腫瘤生長(zhǎng)抑制因子Rb通過(guò)控制能量代謝平衡調(diào)節(jié)細(xì)胞轉(zhuǎn)化作用的機(jī)制研究,。本課題組擬解決Rb是如何控制代謝平衡的及Rb失活的癌細(xì)胞是如何控制代謝失衡的,，并從中找出能特異殺死Rb失活的癌細(xì)胞的分子靶點(diǎn)，為癌癥治療帶來(lái)新方法,、新理念,！
2、研究和代謝相關(guān)的脂肪酸合成,、蛋白質(zhì)合成紊亂(ER Stress)及自噬(Autophagy)發(fā)生的機(jī)制及它們和腫瘤發(fā)生發(fā)展的關(guān)系,。
3、能量代謝如何決定細(xì)胞的命運(yùn),。近些年來(lái),，科學(xué)家們逐漸意識(shí)到幾乎所有的細(xì)胞信號(hào)轉(zhuǎn)導(dǎo)途徑最終都匯集在代謝網(wǎng)絡(luò)上，這迅速催熱了癌癥的代謝研究,。細(xì)胞的代謝是如何決定細(xì)胞命運(yùn)的,？是如何決定細(xì)胞的轉(zhuǎn)化的？我們的研究將著重理清癌細(xì)胞中糖代謝,、脂代謝及蛋白質(zhì)代謝之間的關(guān)系,，尋找癌細(xì)胞得以轉(zhuǎn)化的物質(zhì)基礎(chǔ)(代謝本質(zhì))。
4,、開發(fā)實(shí)時(shí)生物學(xué)功能監(jiān)測(cè)工具,。我們將致力于確定研究細(xì)胞代謝(決定細(xì)胞命運(yùn))的方法；將致力于開發(fā)實(shí)時(shí)監(jiān)測(cè)代謝平衡及細(xì)胞凋亡的工具,。
Research Description
In the past decades, most researchers working on cancer were focusing on cell signal transduction, and they made profound progress in understanding and treating cancers. However, cancer still remains a medical challenge and numerous questions remain to be explored. Metabolic and signal systems in cancer cells can be driven by each other, and they are closely connected but remain relatively independent. Altering the signal transduction network absolutely will drive corresponding metabolic changes, however, most researchers usually complete their studies without investigating metabolic changes, because under these conditions the signal transduction system is positive and it promotes the passive metabolism. On the other hand, when we perturb the metabolic network by targeting metabolic enzymes or changing their substrates concentrations, the signal system also will change. In this setting, the positive metabolic system drives passive signal transduction, nonetheless, we can not always figure out how cancer cells die by the rules of typical signal transduction. The metabolic system probably has its own ways to induce cell death.
Based on our previous studies, we put forward the hypothesis that the irreversible upsetting of metabolic homeostasis can kill cells by some special mechanisms. Cancer cells have many specifically metabolic characteristics that could be rendered as ideal targets for the treatment of cancer. Our future research will be carried out around this hypothesis, and we plan to identify targets to disrupt metabolic homeostasis to kill cancer cells and then dissect their mechanisms.
Project I: Role of Rb in controlling cell proliferation, growth and transformation via regulating redox balance. We want to know how Rb controls cellular stress, and how Rb regulation of cell proliferation, growth and transformation is related to its ability to control cellular stress. In Rb mutant cancer cells, how is Rb inactivation-induced lethal redox imbalance suppressed? This research will help to design strategies to treat cancers holding inactivated Rb.
Project II: Why do cancer cells need to express high level of FAS and how does FAS inhibition kill cancer cells? We will determine the role of FAS hyperactivity in cancer cells, and dissect the mechanism underlying FAS inhibition-induced cell death. Since targeting FAS has been reported to specifically kill cancer cells, many researchers from all over the world are trying to decipher the detailed mechanism but have failed to do so. It seems that it is not possible to explain FAS action in cancer cells by traditional cell signal transduction. We believe the answer will be found in select metabolic pathways that are critical for cancer cell homeostasis. This study is supposed to provide more targets either alone or together with FAS for the treatment of cancers.
Project III: Irreversibly disrupting metabolic homeostasis specifically kills cancer cells. We will determine if metabolic pathways and constituent enzymes play essential roles in maintaining glucose, protein and lipid metabolic homeostasis, and whether they are potential therapeutic targets of cancer cells alone or in combination. We will then dissect the mechanisms by which disruption of metabolic homeostasis leads to cell death. We will set up a highthrough-put screening platform to identify the inhibitors of these pathways/enzymes.
Project IV：Development of novel real-time measuring tools and new biotechnologies. We are trying to set up the research platforms for cancer metabolism and make real-time supervising tools/methods for the biological pathways.
Selected Publications
1,、Tian W., Ma X., Zhang S., Sun Y. and Li B. Fatty Acid Synthase Inhibitors from Plants and Their Potential Application in the prevention of Metabolic Syndrome. Clin Oncol Cancer Res., 8: 1-9. (2011)
2、Li B., Zhao J., Wang CZ, Searle J., He TC., Yuan CS., and Du W. Ginsenoside Rh2 induce apoptosis and paraptosis-like cell death in colon cancer cells through activation p53. Cancer Letters, 28;301(2):185-92. (2011)
3,、Li B., Gordon GM., Du CH., Xu J, and Du W. Specific killing of Rb mutant cancer cells by inactivating TSC2. Cancer Cell, 17: 469-480. (2010)
Highlighted in Science(328: 1455, 2010)
Comments in Cancer Research (70:5198, 2010)
Evaluated in“F1000” by“Faculty Of 1000 Biology”.
4,、Li B., wang CZ., He TC., Yuan CS., and Du W. Antioxidants potentiate American ginseng-induced killing of colorectal cancer cells. Cancer Letters, 289 (1), 62-70. (2010).
5,、Li B., Zhang R., Sun YH., and Tian WX. Inactivation Mechanism of the β-Ketoacyl-[acyl carrier protein] Reductase of Bacterial Type II Fatty Acid Synthase by pigallocatechin Gallate. Biochem. Cell Biol., 84, 755-762 (2006).
6、Li B., Ma XF., and Tian WX. Inhibitory Activity of Chlorogenic Acid on Enzymes Involved in the Fatty Acid Synthesis in Animals and Bacteria. IUBMB Life, 58, 39-46 (2006).
7,、Li B., Ma XF., Wang Y., Wang X., and Tian WX. Structure-Activity Relationships for Polyphenols Inhibiting Animal Fatty Acid Synthase. J. Biochem., 138, 679-686 (2005).
8,、Li B. and Tian WX. Inhibitory Effects of Flavonoids on Animal Fatty Acid Synthase. J. Biochem., 135, 85–91 (2004).
9、Li B. and Tian WX. Presence of Fatty Acid Synthase Inhibitors in the Rhizome of Alpinia officinarum Hance. J. Enzyme Inhib. Med. Chem., 18, 349–356(2003).
（腫瘤細(xì)胞生物學(xué)實(shí)驗(yàn)室）
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