|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Meningeal lymphatic vessels regulate brain tumor drainage and immunity显示文摘Recent studies have shown that meningeal lymphatic vessels(MLVs),which are located both dorsally and basally beneath the skull,provide a route for draining macromolecules and trafficking immune cells from the central nervous system(CNS)into cervical lymph nodes(CLNs),and thus represent a potential therapeutic target for treating neurodegenerative and neuroinflammatory diseases.However,the roles of MLVs in brain tumor drainage and immunity remain unexplored.Here we show that dorsal MLVs undergo extensive remodeling in mice with intracranial gliomas or metastatic melanomas.RNA-seq analysis of MLV endothelial cells revealed changes in the gene sets involved in lymphatic remodeling,fluid drainage,as well as inflammatory and immunological responses.Disruption of dorsal MLVs alone impaired intratumor fluid drainage and the dissemination of brain tumor cells to deep CLNs(dCLNs).Notably,the dendritic cell(DC)trafficking from intracranial tumor tissues to dCLNs decreased in mice with defective dorsal MLVs,and increased in mice with enhanced dorsal meningeal lymphangiogenesis.Strikingly,disruption of dorsal MLVs alone,without affecting basal MLVs or nasal LVs,significantly reduced the efficacy of combined anti-PD-1/CTLA-4 checkpoint therapy in striatal tumor models.Furthermore,mice bearing tumors overexpressing VEGF-C displayed a better response to anti-PD-1/CTLA-4 combination therapy,and this was abolished by CCL21/CCR7 blockade,suggesting that VEGF-C potentiates checkpoint therapy via the CCL21/CCR7 pathway.Together,the results of our study not only demonstrate the functional aspects of MLVs as classic lymphatic vasculature,but also highlight that they are essential in generating an efficient immune response against brain tumors. | Xueting Hu Qiuping Deng Lu Ma Qingqing Li Yidong Chen Yuhan Liao Fan Zhou Chen Zhang Linlin Shao Jun Feng Tubao He Weihai Ning Yan Kong Yingqing Huo Aibin He Bing Liu Jingjing Zhang Ralf Adams Yulong He Fuchou Tang Xiuwu Bian Jincai Luo | 2020 | Cell Research2020，30，3： | 11 |
| 2 | A four-gene signature-derived risk score for glioblastoma:prospects for prognostic and response predictive analyses显示文摘Objective: Glioblastoma(GBM) is the most common primary malignant brain tumor regulated by numerous genes, with poor survival outcomes and unsatisfactory response to therapy.Therefore, a robust, multi-gene signature-derived model is required to predict the prognosis and treatment response in GBM.Methods: Gene expression data of GBM from TCGA and GEO datasets were used to identify differentially expressed genes(DEGs)through DESeq2 or LIMMA methods.The DEGs were then overlapped and used for survival analysis by univariate and multivariate COX regression.Based on the gene signature of multiple survival-associated DEGs, a risk score model was established,and its prognostic and predictive role was estimated through Kaplan–Meier analysis and log-rank test.Gene set enrichment analysis(GSEA) was conducted to explore high-risk score-associated pathways.Western blot was used for protein detection.Results: Four survival-associated DEGs of GBM were identified: OSMR, HOXC10, SCARA3, and SLC39A10.The four-gene signature-derived risk score was higher in GBM than in normal brain tissues.GBM patients with a high-risk score had poor survival outcomes.The high-risk group treated with temozolomide chemotherapy or radiotherapy survived for a shorter duration than the low-risk group.GSEA showed that the high-risk score was enriched with pathways such as vasculature development and cell adhesion.Western blot confirmed that the proteins of these four genes were differentially expressed in GBM cells.Conclusions: The four-gene signature-derived risk score functions well in predicting the prognosis and treatment response in GBM and will be useful for guiding therapeutic strategies for GBM patients. | Mianfu Cao Juan Cai Ye Yuan Yu Shi Hong Wu Qing Liu Yueliang Yao Lu Chen Weiqi Dang XiangZhang Jingfang Xiao Kaidi Yang Zhicheng He Xiaohong Yao Yonghong Cui Xia Zhang Xiuwu Bian | 2019 | Cancer Biology & Medicine2019，16，3： | 2 |
| 3 | Pyroptotic macrophages stimulate the SARS-CoV-2-associated cytokine storm显示文摘Coronavirus disease 2019(COVID-19)is an unprecedented pandemic caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2).As of 22 February 2021,the worldwide pandemic has resulted in more than 110 million cases and 2.4 million deaths.1 Clinical investigation of COVID-19 patients has shown that a systemic cytokine storm can occur,especially in severe cases.2 Treatment of the SARS-CoV-2-associated cytokine storm with tocilizumab3 or anakinra4 has been shown to immediately improve the clinical outcome in most severe and critical COVID-19 patients.These data highlight the systemic cytokine storm as an important exacerbating event in severe COVID-19;however,our understanding of the molecular mechanisms involved in the initiation of the SARS-CoV-2-associated cytokine storm is limited.In the present study,we uncovered a reasonable explanation for cytokine storm initiation through the analysis of 13 autopsy samples from severe COVID-19 patients. | Jinghe Zhang Haibo Wu XiaoHong Yao Dingyu Zhang Yonggang Zhou Binqing Fu Wei Wang Heng Li Zhe Wang Ziming Hu Yong Ren Rui Sun Zhigang Tian Xiuwu Bian Haiming Wei | 2021 | Cellular & Molecular Immunology2021，18，5： | 1 |
| 4 | MicroRNA-137, a HMGA1 Target, Suppresses Colorectal Cancer Cell Invasion and Metastasis in Mice by Directly Targeting FMNL2显示文摘 | Li Liang Xianzheng Li Xiaojing Zhang Zhenbing Lv Guoyang He Wei Zhao Xiaoli Ren Yuling Li Xiuwu Bian Wenting Liao Wei Liu Guangying Yang Yanqing Ding | 2012 | Gastroenterology2012，，： | 1 |
| 5 | Glioma-initiating cells: A predominant role in microglia/macrophages tropism to glioma显示文摘 | Liang Yi Hualiang Xiao Minhui Xu Xianzong Ye Jun Hu Fei Li Mei Li Chunxia Luo Shicang Yu Xiuwu Bian Hua Feng | 2010 | Journal of Neuroimmunology2010，，1： | 1 |
| 6 | Aristolochic acids exposure was not the main cause of liver tumorigenesis in adulthood显示文摘Aristolochic acids(AAs) have long been considered as a potent carcinogen due to its nephrotoxicity. Aristolochic acid I(AAI) reacts with DNA to form covalent aristolactam(AL)-DNA adducts,leading to subsequent A to T transversion mutation, commonly referred as AA mutational signature. Previous research inferred that AAs were widely implicated in liver cancer throughout Asia. In this study, we explored whether AAs exposure was the main cause of liver cancer in the context of HBV infection in China's Mainland. Totally 1256 liver cancer samples were randomly retrieved from 3 medical centers and a refined bioanalytical method was used to detect AAI-DNA adducts. 5.10% of these samples could be identified as AAI positive exposure. Whole genome sequencing suggested 8.41% of 107 liver cancer patients exhibited the dominant AA mutational signature, indicating a relatively low overall AAI exposure rate. In animal models, long-term administration of AAI barely increased liver tumorigenesis in adult mice, opposite from its tumor-inducing role when subjected to infant mice. Furthermore, AAI induced dose-dependent accumulation of AA-DNA adduct in target organs in adult mice, with the most detected in kidney instead of liver. Taken together, our data indicate that AA exposure was not the major threat of liver cancer in adulthood. | Shuzhen Chen Yaping Dong Xinming Qi Qiqi Cao Tao Luo Zhaofang Bai Huisi He Zhecai Fan Lingyan Xu Guozhen Xing Chunyu Wang Zhichao Jin Zhixuan Li Lei Chen Yishan Zhong Jiao Wang Jia Ge Xiaohe Xiao Xiuwu Bian Wen Wen Jin Ren Hongyang Wang | 2022 | Acta Pharmaceutica Sinica B2022，12，5： | 1 |
| 7 | The expression of functional chemokine receptor CXCR4 is associated with the metastatic potential of human nasopharyngeal carcinoma显示文摘 | Jinyue Hu Xiyun Deng Xiuwu Bian | 2005 | Clln Cancer Res2005，11，： | 1 |
| 8 | Formylpeptide Receptor FPR and the Rapid Growth of Malignant Human Gliomas显示文摘 | Ye Zhou Xiuwu Bian Yingying Le et al | 2005 | Journal of the National Cancer Institute2005，11，： | 1 |
| 9 | Establishment of hu-man glioma cellCHG-5 and its biological features显示文摘 | Chen Ziqiang Bian Xiuwu Xin Rong | | 0，，12： | 1 |
| 10 | Potential Significance of Glioma Stem Cells in Angiogenesis and Immuno-pharmacological Therapeutics:Hypothesis and Evidences显示文摘Recent studies on cancer stem cells (CSCs), a special subpopulation of tumor cells, promote our understanding of tumorigenesis, angiogenesis, invasion, drug resistance and recurrence, which establishes new concepts | Xiuwu BIAN | 2009 | 中国肺癌杂志2009，12，6： | 0 |
| 11 | Targeting TRPV1-mediated autophagy attenuates nitrogen mustard-induced dermal toxicity显示文摘Nitrogen mustard(NM)causes severe vesicating skin injury,which lacks effective targeted therapies.The major limitation is that the specific mechanism of NM-induced skin injury is not well understood.Recently,autophagy has been found to play important roles in physical and chemical exposure-caused cutaneous injuries.However,whether autophagy contributes to NM-induced dermal toxicity is unclear.Herein,we initially confrmed that NM dose-dependently caused cell death and induced autophagy in keratinocytes.Suppression of autophagy by 3-methyladenine,chloroquine,and baflomycin A1 or ATG5 siRNA attenuated NM-induced keratinocyte cell death.Furthermore,NM increased transient receptor potential vanilloid 1(TRPV1)expression,intracellular Ca2+content,and the activities of Car+/calmodulin-dependent kinase kinaseβ(CaMKKB),AMP-activated protein kinase(AMPK),unc-51-like kinase 1(ULK1),and mammalian target of rapamycin(mTOR).NM-induced autophagy in keratinocytes was abolished by treatment with inhibitors of TRPV1(capsazepine),CaMKKβ(STO-609),AMPK(compound C),and ULK1(SBI-0206965)as well as TRPV1,CaMKKB,and AMPK siRNA transfection.In addition,an mTOR inhibitor(rapamycin)had no signifcant effect on NM-stimulated autophagy or cell death of keratinocytes.Finally,the results of the in vivo experiment in NM-treated skin tissues were consistent with the findings of the in vitro experiment.In conclusion,NM-caused dermal toxicity by overactivating autophagy partially through the activation of TRPV1-Ca2+-CaMKKB-AMPK-ULK1 signaling pathway.These results suggest that blocking TRPV1-dependent autophagy could be a potential treatment strategy for NM-caused cutaneous injury. | Mingliang Chen Xunhu Dong Haoyue Deng Feng Ye Yuanpeng Zhao Jin Cheng Guorong Dan Jiqing Zhao Yan Sai Xiuwu Bian Zhongmin Zou | 2021 | Signal Transduction and Targeted Therapy2021，6，2： | 0 |
| 12 | Highly pathogenic coronavirus N protein aggravates inflammation by MASP-2-mediated lectin complement pathway overactivation显示文摘Excessive inflammatory responses contribute to the pathogenesis and lethality of highly pathogenic human coronaviruses,but the underlying mechanism remains unclear.In this study,the N proteins of highly pathogenic human coronaviruses,including severe acute respiratory syndrome coronavirus(SARS-CoV),middle east respiratory syndrome coronavirus(MERS-CoV)and severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),were found to bind MASP-2,a key serine protease in the lectin pathway of complement activation,resulting in excessive complement activation by potentiating MBL-dependent MASP-2 activation,and the deposition of MASP-2,C4b,activated C3 and C5b-9.Aggravated inflammatory lung injury was observed in mice infected with adenovirus expressing the N protein.Complement hyperactivation was also observed in SARS-CoV-2-infected patients.Either blocking the N protein:MASP-2 interaction,MASP-2 depletion or suppressing complement activation can significantly alleviate N protein-induced complement hyperactivation and lung injury in vitro and in vivo.Altogether,these data suggested that complement suppression may represent a novel therapeutic approach for pneumonia induced by these highly pathogenic coronaviruses. | Ting Gao Lin Zhu Hainan Liu Xiaopeng Zhang Tingting Wang Yangbo Fu Hongzhen Li Qincai Dong Yong Hu Zhang Zhang Jing Jin Zijing Liu Weihong Yang Yaoning Liu Yanwen Jin Kaitong Li Yongjiu Xiao Junli Liu Huailong Zhao Yue Liu Ping Li Jibo Song Lu Zhang Yuwei Gao Sisi Kang Shoudeng Chen Qingjun Ma Xiuwu Bian Wei Chen Xuan Liu Qing Mao Cheng Cao | 2022 | Signal Transduction and Targeted Therapy2022，7，10： | 0 |
| 13 | Bottlenecks and opportunities in immunotherapy for glioma:a narrative review显示文摘Glioma is the most aggressive brain tumor having invasive ability and a highly heterogeneous phenotype.Many patients with glioma respond poorly to traditional surgery or temozolomide-based chemotherapy.Over the past few decades,developments in immunotherapeutic strategies have provided newer insights into the treatment of gliomas.Immunotherapy is based on the principle of normalization or recovery of T cell-mediated anti-tumor immunoreaction.Different innovative strategies have been used;these include enhancement of immunogenicity by administration of tumor antigens or dendritic cell vaccines,replenishment of cytotoxic T cells by adoptive T cell transfer,repair of exhausted T cells by immune checkpoint inhibitors,and the use of other immune activators such as oncolytic viruses.However,many immunotherapy-based clinical trials did not meet the expected therapeutic endpoints in patients with glioma.Gliomas use unique strategies to generate an immune-suppressive microenvironment;these include limiting immunogenicity and repressing T cell infiltration or activation.This may be addressed by the incorporation of immunotherapy with standard therapy or by use of certain innovative approaches such as tumor-treating fields.In this review,we summarize the updated immunotherapies in glioma and discuss current limitations and future prospects. | Ying Shi Mengwan Wu Yuyang Liu Ling Chen Xiuwu Bian Chuan Xu | 2022 | Journal of Bio-X Research2022，5，4： | 0 |
| 14 | Effects of Nordy on the proliferation, differentiation,and apoptosis of HPV16 subgene-immortalized human endocervical cells显示文摘Objective The aim of this study was to investigate the effects of Nordy on the proliferation, differentiation, and apoptosis of HPV16 subgene-immortalized human endocervical cells(H8 cells).Methods After treatment with Nordy, H8 cell proliferation was evaluated using the MTT assay. The effects of Nordy on the cell cycle and apoptosis of H8 cells were analyzed by flow cytometry(FCM) and the Annexin V-FITC method. H8 cell MCM5 expression was detected by immunocytochemistry. Morphological changes were observed by light and electron microscopy. Telomerase activity was evaluated by TRAP-ELISA.Results We found that 10 μmol/L–100 μmol/L Nordy significantly inhibited H8 cell proliferation. After treatment with Nordy, H8 cells were blocked in the G0/G1 phase, and the rate of cell apoptosis increased significantly. Cells differentiated toward innocuousness, and MCM5 expression and telomerase activity notably decreased.Conclusion Nordy was observed to inhibit proliferation and promote apoptosis in H8 cells. Nordy also induced H8 cell differentiation; this effect may have been achieved by blocking the cell cycle and decreasing telomerase activity. | Wei Chen Yong Zhao Xiuwu Bian | 2018 | Oncology and Translational Medicine2018，4，1： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员