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Role of apoptosis resistance in immune evasion and metastasis of colorectal cancer

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World Journal of Gastrointestinal Oncology 2010年第11期2卷 399-406页

作者： Kebin Liu, Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Health Sciences University, Augusta, GA 30912, United States Kebin Liu Department of Biochemistry and Molecular Biology Medical College of Georgia Georgia Health Sciences University Augusta GA 30912 United States.

The host immune system functions as a guardian against tumor development. It has been demonstrated that cytotoxic T lymphocyte (CTL)-mediated cytotoxic pathways function to inhibit or delay human colorectal cancer development. However, the host anti-tumor immune responses also 'edit' the tumor and select for more aggressive variants, resulting in immune evasion and tumor escape. Fas is a death receptor that mediates one of the major cytotoxic effector mechanisms of the CTLs. Fas is highly expressed in normal human colon epithelial cells but is frequently silenced in colorectal carcinoma, especially in metastatic colorectal carcinoma, suggesting that loss of Fas expression and function may be an immune evasion and tumor escape mechanism. In addition, recent studies indicated that Fas also mediates cellular proliferation signaling pathways to promote tumor development. Therefore, the death receptor Fas may not only transduce death signals to suppress tumor development but also activate cellular proliferation and the migration process to promote tumor growth and progression. Thus, understanding the mechanisms by which the Fas receptor and its associated protein complex transduces the death and survival signals may identify molecular targets for the development of therapeutic strategy to enhance the Fas-mediated death signals to increase the efficacy of cancer immunotherapy.

关键词： Apoptosis Fas Metastasis Immune evasion

Viral evasion of DNA-stimulated innate immune responses

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Cellular & Molecular Immunology 2017年第1期14卷 4-13页

作者： Maria H Christensen Sфren R Paludan Department of Biomedicine Aarhus University Aarhus DK-8000 Denmark Aarhus Research Center for Innate Immunology Aarhus University Aarhus DK-8000 Denmark

Cellular sensing of virus-derived nucleic acids is essential for early defenses against virus infections. In recent years, the discovery of DNA sensing proteins, including cyclic GMP-AMP synthase （cGAS） and gamma-interferon- inducible protein （IFI16）, has led to understanding of how cells evoke strong innate immune responses against incoming pathogens carrying DNA genomes. The signaling stimulated by DNA sensors depends on the adaptor protein STING （stimulator of interferon genes）, to enable expression of antiviral proteins, including type I interferon. To facilitate efficient infections, viruses have evolved a wide range of evasion strategies, targeting host DNA sensors, adaptor proteins and transcription factors. In this review, the current literature on virus-induced activation of the STING pathway is presented and we discuss recently identified viral evasion mechanisms targeting different steps in this antiviral pathway.

关键词： DNA sensing evasion innate immunology STING

Explicitness evasion with Humor under Cooperative Principle

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海外英语 2016年第6期 189-190页

作者：吴劼 Jilin University

Explicitness evasion in communication is like lube that avoids hurting the other party's feeling. It lubricates human relationship in communication and helps to save face of communicators. Too much conversational explicitness is easy to give rise to misunderstandings even if it is for good intentions. And when the divergence among two parties become exacerbated, the conflict or even fighting will arise as a result. So to create a light-hearted conversational atmosphere, explicitness evasion, an aesthetic speech art, is deeply thought-provoking. Therefore, this study attempts to touch on the validity of applying humor under Cooperative Principle to the explicitness evasion. Hopefully, readers can better understand how to avoid hurting others inadvertently when speaking and how to achieve successful conversations. Moreover, it can help practitioners to find some sound methods to combine speech and humanity together to make them harmonious in the long run.

关键词： explicitness evasion humor Cooperative Principle

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雪铁龙evasion遨游

汽车维修 2001年第6期 36-36页

雪铁龙遨游车为想利用各种方式“出门旅游”的人提供一个最佳的野外交通工作。雪铁龙evasion(遨游)车是一辆马力大、行驶性能极佳的理想轿车。这种宽敞、用途无限广、非常舒适、高雅大方的单厢车是为休闲、长途旅行、各种来往的需要而... 详细信息

雪铁龙遨游车为想利用各种方式“出门旅游”的人提供一个最佳的野外交通工作。雪铁龙evasion(遨游)车是一辆马力大、行驶性能极佳的理想轿车。这种宽敞、用途无限广、非常舒适、高雅大方的单厢车是为休闲、长途旅行、各种来往的需要而设计制造的。

关键词：雪铁龙 evasion 制动盘加速时间长途旅行立方分米

Japanese Encephalitis Virus NS1' Protein Antagonizes Interferon Beta Production

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Virologica Sinica 2018年第6期33卷 515-523页

作者： Dengyuan Zhou Fan Jia Qiuyan Li Luping Zhang Zheng Chen Zikai Zhao Min Cui Yunfeng Song Huanchun Chen Shengbo Cao Jing Ye State Key Laboratory of Agricultural Microbiology Huazhong Agricultural University Key Laboratory of Preventive Veterinary Medicine in Hubei Province College of Veterinary Medicine Huazhong Agricultural University The Cooperative Innovation Center for Sustainable Pig Production Huazhong Agricultural University Wuhan Institute of Physics and Mathematics (WIPM) Chinese Academy of Sciences

Japanese encephalitis virus(JEV) is a mosquito-borne virus and the major cause of viral encephalitis in Asia. NS1', a52-amino acid C-terminal extension of NS1, is generated with a-1 programmed ribosomal frameshift and is only present in members of the Japanese encephalitis serogroup of flaviviruses. Previous studies demonstrated that NS1' plays a vital role in virulence, but the mechanism is unclear. In this study, an NS1' defected(rG66A) virus was generated. We found that rG66A virus was less virulent than its parent virus(pSA14) in wild-type mice. However, similar mortality caused by the two viruses was observed in an IFNAR knockout mouse model. Moreover, we found that rG66A virus induced a greater type Ⅰ interferon(IFN) response than that by pSA14, and JEV NS1' significantly inhibited the production of IFN-b and IFN-stimulated genes. Taken together, our results reveal that NS1' plays a vital role in blocking type I IFN production to help JEV evade antiviral immunity and benefit viral replication.

关键词： Japanese encephalitis virus(JEV) NS1’ Type Ⅰ interferon(IFN-Ⅰ) Immune evasion

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Mechanisms of drug resistance in colon cancer and its therapeutic strategies

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World Journal of Gastroenterology 2016年第30期22卷 6876-6889页

作者： Tao Hu Zhen Li Chun-Ying Gao Chi Hin Cho School of Biomedical Sciences Faculty of Medicine the Chinese University of Hong Kong Hong Kong China Department of Biostatistics Graduate School of Public Health University of Pittsburgh Pittsburgh PA 15261 United States Department of Pharmaceutics School of Pharmacy University of Washington Seattle WA 98195 United States School of Pharmacy Southwest Medical University Luzhou 646000 Sichuan Province China

Drug resistance develops in nearly all patients with colon cancer, leading to a decrease in the therapeutic efficacies of anticancer agents. This review provides an up-to-date summary on over-expression of ATPbinding cassette(ABC) transporters and evasion of apoptosis, two representatives of transport-based and non-transport-based mechanisms of drug resistance, as well as their therapeutic strategies. Different ABC transporters were found to be up-regulated in colon cancer, which can facilitate the efflux of anticancer drugs out of cancer cells and decrease their therapeutic effects. Inhibition of ABC transporters by suppressing their protein expressions or co-administration of modulators has been proven as an effective approach to sensitize drug-resistant cancer cells to anticancer drugs in vitro. On the other hand, evasion of apoptosis observed in drug-resistant cancers also results in drug resistance to anticancer agents, especially to apoptosis inducers. Restoration of apoptotic signals by BH3 mimetics or epidermal growth factor receptor inhibitors and inhibition of cancer cell growth by alternative cell death pathways, such as autophagy, are effective means to treat such resistant cancer types. Given that the drug resistance mechanisms are different among colon cancer patients and may change even in a single patient at different stages, personalized and specific combination therapy is proposed to be more effective and safer for the reversal of drug resistance in clinics.

关键词： Colon cancer Drug resistance ATP-binding cassette transporters evasion of apoptosis Autophagy

Bioinformatics analysis for structure and function of CPR of Plasmodium falciparum

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Asian Pacific Journal of Tropical Medicine 2011年第2期4卷 85-87页

作者： Zhigang Fan Lingmin Zhang Guogang Yan Qiang Wu Xiufeng Gan Saifeng Zhong Guifen Lin School of Troptical and Laboratory Medicine Hainan Medical University Department of Parasitology Medical SchoolJinan University School of Nursing Hainan Medical University

Objective:To analyse the structure and function of NADPH-cytochrome p450 reductase(CYPOR or CPR) from Plasmodium falciparum(Pf),and to predict its’ drug target and vaccine target. Methods:The structure,function,drug target and vaccine target of CPR from Plasmodium falciparum were analyzed and predicted by bioinformatics ***:PfCPR,which was older CPR,had close relationship with the CPR from other Plasmodium species,but it was distant from its hosts,such as Homo sapiens and *** was located in the cellular nucleus of Plasmodium falciparum.335aa-352aa and 591aa - 608aa were inserted the interior side of the nuclear membrane,while 151aa-265aa was located in the nucleolus organizer *** had 40 function sites and 44 protein-protein binding sites in amino acid *** teriary structure of laa-700aa was forcep-shaped with wings.15 segments of PfCPR had no homology with Homo sapien CPR and most were exposed on the surface of the *** segments had 25 protein-protein binding *** 13 other segments all possessed function sites. Conclusions:The evolution or genesis of Plasmodium falciparum is earlier than those of Homo *** is a possible resistance site of antimalarial drug and may involve immune evasion, which is associated with parasite of sporozoite in *** is unsuitable as vaccine target,but it has at least 13 ideal drug targets.

关键词： Plasmodium falciparum NADPH-cytochrome p450 reductase Origin Immune evasion Drug target Vaccine target

Hepatitis B virus-persistent infection and innate immunity defect: Cell-related or virus-related?

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World Journal of Clinical Cases 2018年第9期6卷 233-241页

作者： Jian Tang Zhen-Yu Wu Rong-Juan Dai Jing Ma Guo-Zhong Gong Department of Infectious Disease the Second Xiangya Hospital Central South University Department of Infectious Disease the First Affiliated Hospital of University of South China

The outcomes of hepatitis B virus(HBV) infection are closely related to the age at which infection was acquired. Infection acquired in adult life tends to be selflimited, in contrast to perinatal acquirement, for which chronic persistence of the HBV is a general outcome. Innate immunity plays an indispensable role in early virus infection, facilitating virus clearance. However, it has been reported that HBV is under-recognized and poorly eliminated by the innate immune system in the early stages of infection, possibly explaining the long-lasting persistence of viremia afterwards. Furthermore, due to the existence of covalently closed circular DNA, chronic HBV clearance is very difficult, even when patients are given interferon-α and nucleotide/nucleoside analogs for antiviral therapy. The mechanism by which HBV evades innate immune recognition and establishes persistent infection remains a subject of debate. Besides, some researchers are becoming more interested in how to eradicate chronic HBV infection by restoring or boosting innate immunity. This review aimed to summarize the current knowledge on how intrahepatocyte signaling pathways and innate immune cells act after the onset of HBV infection and how these actions are related to the persistence of HBV. We anticipate the insights presented herein to be helpful for future development of novel immune therapeutic strategies to fight HBV infection.

关键词： Hepatitis B virus Innate immunity Immune evasion Pattern recognition receptor Toll-like receptor Natural killer cells Kupffer cells Dendritic cells

Natural killer cells in hepatitis C:Current progress

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World Journal of Gastroenterology 2016年第4期22卷 1449-1460页

作者： Joo Chun Yoon Chang Mo Yang Youkyong Song Jae Myun Lee Department of Microbiology and Tissue Injury Defense Research Center Ewha Womans University School of MedicineSeoul 158-710South Korea Department of Microbiology Yonsei University College of MedicineSeoul 120-752South Korea

Patients infected with the hepatitis C virus(HCV) are characterized by a high incidence of chronic infection, which results in chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. The functional impairment of HCV-specific T cells is associated with the evolution of an acute infection to chronic hepatitis. While T cells are the important effector cells in adaptive immunity, natural killer(NK) cells are the critical effector cells in innate immunity to virus infections. The findings of recent studies on NK cells in hepatitis C suggest that NK cell responses are indeed important in each phase of HCV infection. In the early phase, NK cells are involved in protective immunity to HCV. The immune evasion strategies used by HCV may target NK cells and might contribute to the progression to chronic hepatitis C. NK cells may control HCV replication and modulate hepatic fibrosis in the chronic phase. Further investigations are, however, needed, because a considerable number of studies observed functional impairment of NK cells in chronic HCV infection. Interestingly, the enhanced NK cell responses during interferon-α-based therapy of chronic hepatitis C indicate successful treatment. In spite of the advances in research on NK cells in hepatitis C, establishment of more physiological HCV infection model systems is needed to settle unsolved controversies over the role and functional status of NK cells in HCV infection.

关键词： Hepatitis C virus Natural killer cell Accessorycell Virus-host interaction Immune evasion Acutehepatitis Chronic hepatitis Treatment response