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The Gut Microbiota, Tumorigenesis, and Liver Diseases

Engineering 2017年第1期3卷 110-114页

作者： guishuai lv Ningtao Cheng Hongyang Wang International Cooperation Laboratory on Signal Transduction Eastern Hepatobiliary Surgery Institute Second Military Medical University Shanghai 200438 China National Center for Liver Cancer Shanghai 201805 China

In recent decades, diseases concerning the gut microbiota have presented some of the most serious public health problems worldwide. The human host＇s physiological status is influenced by the intestinal microbiome, thus integrating external factors, such as diet, with genetic and immune signals. The notion that chronic inflammation drives carcinogenesis has been widely established for various tissues. It is surprising that the role of the microbiota in tumorigenesis has only recently been recognized, given that the presence of bacteria at tumor sites was first described more than a century ago. Extensive epidemiological studies have revealed that there is a strong link between the gut microbiota and some common cancers. However, the exact molecular mechanisms linking the gut microbiota and cancer are not yet fully understood. Changes to the gut microbiota are instrumental in determining the occurrence and progression of hepatocarcinoma, chronic liver diseases related to alcohol, nonalcoholic fatty liver disease （NAFLD）, and cirrhosis. To be specific, the gut milieu may play an important role in systemic inflammation, endotoxemia, and vasodilation, which leads to complications such as spontaneous bacterial peritonitis and hepatic encephalopathy. Relevant animal studies involving gut microbiota manipulations, combined with observational studies on patients with NAFLD, have provided ample evidence pointing to the contribution of dysbiosis to the pathogenesis of NAFLD. Given the poor prognosis of these clinical events, their prevention and early management are essential. Studies of the composition and function of the gut microbiota could shed some light on understanding the prognosis because the microbiota serves as an essential component of the gut milieu that can impact the aforementioned clinical events. As far as disease management is concerned, probiotics may provide a novel direction for therapeutics for hepatocellular carcinoma （HCC） and NAFLD, given that probioti

关键词： Gut microbiota Dysbiosis Tumorigenesis Hepatocellular carcinoma Nonalcoholic fatty liver disease

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MXR7 facilitates liver cancer metastasis via epithelial-mesenchymal transition

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Science China(Life Sciences) 2017年第11期60卷 1203-1213页

作者： guishuai lv yexiong tan hongwei lv tian fang changzheng wang ting li yanting yu congli hu wen wen hongyang wang wen yang international cooperation laboratory on signal transduction eastern hepatobiliary surgery institutesecond military medical universityShanghai 200438China national center for liver cancer Shanghai 201805China state key laboratory of oncogenes and related genes shanghai cancer institute renji hospitalshanghai jiaotong university school of medicineShanghai 200127China

MXR7 is a cell-surface protein and highly expressed in hepatocellular carcinoma(HCC). The aim of this study is to determine the expression profile of MXR7 in HCC and investigate the influence of MXR7 on invasion and metastasis of HCC cells. For this purpose, immunohistochemical assay was used to identify the differential expression of MXR7 in 94 HCC specimens. Expression of MXR7 in 4 pairs of HCC and portal vein tumor thrombus(PVTT) was also tested. The motility of HCC cells were characterized by transwell migration and matrigel invasion assays. In vivo metastasis potential was determined via tail vein injection ***, compared with noninvasive HCC tumors or human HCC cell lines with low metastatic potential, invasive HCC samples and HCC cell lines with high metastatic potential exhibited higher MXR7 expression. Furthermore, forced expression of MXR7 in SMMC-7721 promoted cell proliferation, migration and invasion in vitro and accelerated tumor growth and metastasis in vivo. Conversely, knockdown of MXR7 expression in HuH7 cells inhibited proliferation and motility of cells. Mechanically,overexpression of MXR7 promoted epithelial-mesenchymal transition(EMT) progress, and MXR7 depletion repressed the EMT phenotype. In conclusion, MXR7 is a mediator of EMT and metastasis in HCC and may serve as a novel therapeutic target.

关键词： hepatocellular carcinoma(HCC) MXR7 metastasis epithelial-mesenchymal transition(EMT)

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肝癌的生物治疗

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中华肝脏病杂志 2015年第6期23卷 401-403页

作者：吕桂帅谈冶雄王红阳国家肝癌科学中心第二军医大学东方肝胆外科医院上海200438

肝细胞癌（HCC）是全球病死率最高的恶性肿瘤之一.我国每年约有38.3万人死于肝癌,约占全球肝癌死亡病例数的51％[1].生物治疗作为现代肿瘤综合治疗的一种新模式,在肝癌治疗中的作用和地位越来越受到重视.生物治疗的概念非常广泛,包括靶... 详细信息

肝细胞癌（HCC）是全球病死率最高的恶性肿瘤之一.我国每年约有38.3万人死于肝癌,约占全球肝癌死亡病例数的51％[1].生物治疗作为现代肿瘤综合治疗的一种新模式,在肝癌治疗中的作用和地位越来越受到重视.生物治疗的概念非常广泛,包括靶向治疗、免疫治疗、基因治疗等,本文重点讨论肝癌生物治疗领域近期已进入临床应用或进入临床研究阶段的重要进展.

关键词：肝肿瘤免疫疗法生物治疗靶向治疗

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