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1.
Journal of Sun Yat-sen University(Medical Sciences) ; (6): 7-15, 2020.
Article in Chinese | WPRIM | ID: wpr-817626

ABSTRACT

@#Anti-cancer targeted therapy “(targeted” cancer therapy) is the use of small molecule drugs or antibodies themselves, guided by specific targeting tools, to attack tumor cells and their microenvironment or activate the body’s immune response. The rapid development of targeted therapy has enabled specific anti- tumor therapies to be achieved, which has taken us another step closer to our ultimate goal of treating tumors, that is, to effectively kill tumors without harming normal tissues. This article reviews the related contents of tumor targeted therapy, such as tumor-associated antigens, antibodies, and targeting strategies and also elaborates on the research in this field in combination with the study of our team.

2.
Journal of Sun Yat-sen University(Medical Sciences) ; (6): 228-236, 2019.
Article in Chinese | WPRIM | ID: wpr-817738

ABSTRACT

@#【Objective】 To use high- throughout sequencing technologies for examining differentially expressed long non-coding RNA(lncRNA)in human umbilical vein endothelial cell(HUVEC)infected by dengue virus type Ι(DENV-1), to analyze and explore the potential molecular mechanisms of HUVEC dysfunction or damage.【Methods】After 24 hours of DENV-1 infection,RNA samples were extracted from control groups and viral groups. Sequencing and the differentially expressed lncRNAs were screened ,and then GO and KEGG enrichment analysis were conducted and a co- expression network map was constructed.【Results】In contrast to the control group,there were 2 623 lncRNA expressed differently, among which 1 441 were up-regulated,while 1 182 were down-regulated. It was found that the differentially expressed lncRNA and the predicted corresponding target genes were mainly distributed in the regions of biological processes of antigen presentation,interferon synthesis,apoptosis and cell adhesion. 【Conclusion】After HUVEC were infected with DENV-1,lncRNA expression profile changes significantly,which is closely related to the occurrence and development of dengue hemorrhagic fever/dengue shock syndrome(DHF/DSS).

3.
Chinese journal of integrative medicine ; (12): 540-545, 2014.
Article in English | WPRIM | ID: wpr-262635

ABSTRACT

<p><b>OBJECTIVE</b>To observe the anti-virus effects of andrographolide (AD) on the retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) signaling pathway when immunological cells were infected with H1N1.</p><p><b>METHODS</b>Leukomonocyte was obtained from umbilical cord blood by Ficoll density gradient centrifugation, and immunological cells were harvested after cytokines stimulation. Virus infected cell model was established by H1N1 co-cultured with normal human bronchial epithelial cell line (16HBE). The optimal concentration of AD was defined by methyl-thiazolyl-tetrazolium (MTT) assay. After the virus infected cell model was established, AD was added into the medium as a treatment intervention. After 24-h co-culture, cell supernatant was collected for interferon gamma (IFN-γ) and interleukin-4 (IL-4) enzyme-linked immunosorbent assay (ELISA) detection while immunological cells for real-time polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The optimal concentration of AD for anti-virus effect was 250 μg/mL. IL-4 and IFN-γ in the supernatant and mRNA levels in RLRs pathway increased when cells was infected by virus, RIG-I, IFN-β promoter stimulator-1 (IPS-1), interferon regulatory factor (IRF)-7, IRF-3 and nuclear transcription factor κB (NF-κB) mRNA levels increased significantly (P<0.05). When AD was added into co-culture medium, the levels of IL-4 and IFN-γ were lower than those in the non-interference groups and the mRNA expression levels decreased, RIG-I, IPS-1, IRF-7, IRF-3 and NF-κB decreased significantly in each group with significant statistic differences (P<0.05).</p><p><b>CONCLUSIONS</b>The RLRs mediated viral recognition provided a potential molecular target for acute viral infections and andrographolide could ameliorate H1N1 virus-induced cell mortality. And the antiviral effects might be related to its inhibition of viral-induced activation of the RLRs signaling pathway.</p>


Subject(s)
Humans , Adaptor Proteins, Signal Transducing , Genetics , Metabolism , Antiviral Agents , Pharmacology , Cells, Cultured , Coculture Techniques , DEAD Box Protein 58 , DEAD-box RNA Helicases , Genetics , Metabolism , Dendritic Cells , Allergy and Immunology , Virology , Diterpenes , Pharmacology , Fetal Blood , Cell Biology , Influenza A Virus, H1N1 Subtype , Allergy and Immunology , Influenza, Human , Drug Therapy , Allergy and Immunology , Virology , Interferon-beta , Genetics , Metabolism , Interferon-gamma , Metabolism , Interleukin-4 , Metabolism , Leukocytes, Mononuclear , Allergy and Immunology , Virology , Macrophages , Virology , NF-kappa B , Genetics , Metabolism , Promoter Regions, Genetic , Allergy and Immunology , RNA, Messenger , Metabolism , Signal Transduction , Genetics , Allergy and Immunology
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