7月5日15:00 [学术报告] Overcoming Multidrug Resistance by Nanodrugs

发布时间:2023-05-30 | 【打印】 【关闭】

时    间:202375日(星期三) 15:00

    点:国家纳米科学中心  新科研楼第六会议室

报告人:陈哲生教授Drug Resistance Updates主编,圣大生物技术研究院院长

报告题目:Overcoming Multidrug Resistance by Nanodrugs

邀请人:梁兴杰


个人简介:

陈哲生教授1985年于广东药科大学获公共卫生学学士学位,1988年于中山医科大学获得毒理学硕士学位,1998年于日本鹿儿岛大学获得药理学博士学位,1998-2000担任日本科学技术振兴会外国人特别研究员,2000-2004年在美国Fox Chase癌症中心从事博士后研究,2004年至今担任美国圣约翰大学药学系肿瘤药理室主任和博士生导师,并于2010年获得终身教授。陈教授是圣大的生物技术研究院院长。陈教授是肿瘤耐药逆转研究领域的著名学者,主要从事肿瘤耐药机制及其耐药逆转剂的研究,致力于克服肿瘤多药耐药的研究。已在Chemical Society of Review, Advanced MaterialsNature Communications, Advanced Science, Molecular Cancer, Signal Transduction and Targeted Therapy, Drug Resistance Updates, Cancer Research, Clinical Cancer Research 等专业期刊发表SCI论文~460多篇. 他的文章被引用超过2.5万次,H-index77. 他获美国发明专利2项、中国发明专利5项,撰写英文著作15部,应邀在国际大会和学术机构作学术报告~300多次。现担任Drug Resistance Updates, Recent Patents on Anticancer Drug Discovery 等杂志的主编,及其他27个杂志的编委和200多个杂志的审稿人。他也是中国自然科学基金,美国NIH基金,法国,新西兰,匈牙利,波兰,荷兰,加拿大与香港等国家与地区基金的评审专家。他还是中山大学附属七院,广州医科大学,潍坊医学院等大学的特聘/客座教授。他于1997年获得香港第五届肿瘤国际大会青年科学家奖和日本安田医学生优秀奖, 2003年美国癌症学会(AACR)青年科学家奖,2011年获圣约翰大学优秀科研奖,2016获圣约翰大学突出成就奖等。自从2004年,他已14次获得圣约翰大学优秀教师奖。

 

报告内容:

   We have used varieties of nanomaterials, such as tea nanoparticles and lipid-saparin nanuparticles to overcome drug resistance in cancer. Recently, the synthesis and the evaluation of the efficacy of a cycloruthenated complex, RuZ, was reported, to overcome multi-drug resistance (MDR) in cancer cells. RuZ can self-assemble into nanoaggregates in the cell culture medium, resulting in a high intracellular concentration of RuZ in MDR cancer cells. The self-assembly significantly decreases oxygen consumption and inhibits glycolysis, which decreases cellular adenosine triphosphate (ATP) levels. The decrease in ATP levels and its low affinity for the ABCB1 and ABCG2 transporters (which mediate MDR) significantly increase the retention of RuZ by MDR cancer cells. Furthermore, RuZ increases cellular oxidative stress, inducing DNA damage, and, in combination with the aforementioned effects of RuZ, increases the apoptosis of cancer cells. Proteomic profiling analysis suggests that the RuZ primarily decreases the expression of proteins that mediate glycolysis and aerobic mitochondrial respiration and increases the expression of proteins involved in apoptosis. RuZ inhibits the proliferation of 35 cancer cell lines, of which 7 cell lines are resistant to clinical drugs. It is also active in doxorubicin-resistant MDA-MB-231/Adr mouse tumor xenografts. To the best of our knowledge, the results are the first to show that self-assembled cycloruthenated complexes are efficacious in inhibiting the growth of MDR cancer cells.