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重庆大学附属肿瘤医院肿瘤内科--李咏生

李咏生
李咏生 教授/主任医师

重庆大学附属肿瘤医院肿瘤内科

【个人简介】

美国哈佛医学院博士后,现任重庆大学附属肿瘤医院肿瘤内科教授、博士生导师、主任医师,兼任陆军军医大学博士生导师,美国哈佛医学院博士后,现任重庆大学附属肿瘤医院肿瘤内科教授、博士生导师、主任医师,兼任陆军军医大学博士生导师,海外高层次人才、重庆市杰出青年基金获得者、、中国临床肿瘤学会CSCO首批“35岁以下最具潜力青年肿瘤医生”入选者、国家自然科学基金二审专家肿瘤组副组长、重庆市学术技术带头人、重庆市首批“青年专家工作室”领衔专家、重庆市高校创新研究群体负责人。主持国家自然科学基金重点国际合作项目、面上项目等课题12项,经费2000余万元,发表文章60余篇,累计影响因子(IF)大于300,以第一/通信作者在Immunity、Ann Rheum Dis、Sci Adv、Nat Commun、STTT、J Hematol Oncol、Cancer Res等杂志共发表SCI论文30余篇,论文被Nature、Science、Cell、PNAS等著名杂志引用3000余次,多篇论文被F1000收录。任中国抗癌协会肿瘤代谢专委会免疫代谢学组组长、中国抗癌协会肿瘤与微生态专委会常务委员、重庆市免疫学会代谢免疫专委会主任委员、重庆市医学会精准医疗与分子诊断专委会副主任委员;美国免疫学家协会(AAI)、美国微生物学会(ASM)、美国癌症研究协会(AACR)、欧洲肿瘤免疫协会(EATI)会员;Frontiers in Immunology副编辑;STTT、Cancer Research、Theranostics、Critical Care Medicine、J Hematol Oncol等20多个SCI杂志特邀审稿人。

精彩报告

2020-11-03 “肿瘤代谢与微环境”主题网络研讨会(2020)
报告:STIM1 is a metabolic checkpoint that programs tumorigenesis and metastasis in HCC 报名占位
【摘要】 Cancer cells possess anabolic pathways to acquire energy and material basis for rapid tumor growth, while the metastatic tumor cells prefer catabolic metabolism to survive under metabolic stress. However, the metabolic reprogramming in cancer cells orchestrating tumorigenesis and metastasis is unknown. Here, we show that stromal interaction molecule 1 (STIM1), an endoplasmic reticulum (ER) Ca2+ sensor, mediates dynamic metabolic-switching during the tumorigenesis and metastasis of hepatocellular carcinoma (HCC). During tumorigenesis, STIM1 correlates with elevated HIF-1α in hypoxic HCC and is upregulated during tumor growth. HIF-1 transcripts STIM1 and promotes store-operated calcium entry (SOCE), which in return contributes to the stabilization of HIF-1α by activating Ca2+ /calmodulin-dependent protein kinase II (CaM kinase II or CaMKII) and p300 in hypoxic HCC cells. Moreover, STIM1-deficiency inhibits cell proliferation via repressing HIF-1-dependent anabolic metabolism, such as glucose uptake, glycolysis and fatty acid synthesis (FAS), while activates LKB1(Liver kinase B1)/AMPK(AMP-activated protein kinase)-dependent fatty acid oxidation (FAO). Of interest, STIM1 is significantly down-regulated in invasion-edge compared to the corresponding center region of HCC tumor tissue, as well as decreased in several epithelial-mesenchymal transition (EMT) models of HCC cells. Bioinformatics analysis reveals that low expression of STIM1 is closely associated with poor-survival of HCC patients. Mechanistically, STIM1 stabilizes Snai1 by activating SOCE/CaMKII/PI3K/GSK3β signaling cascade during carcinogenesis, whereas Snai1 transcriptionally suppresses STIM1 expression and represses SOCE during EMT. Low concentration of SOCE inhibitor SKF96365 notably promotes the metastasis and anoikis-resistance of Snai1 O/E-cells. On the contrary, restoration of STIM1 dramatically diminishes the anoikis-resistance and metastatic ability. These cells exhibit reduced anabolic metabolism and activated FAO induced by Snai1-O/E in HCC cells. These results suggest that STIM1 is a metabolic checkpoint that programs tumorigenesis and metastasis of HCC via temporally regulating the anabolic/catabolic balance to meet the dynamic metabolic requirements.

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