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您的检索式：作者名="Caijun Zha"
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| 1 | Neutrophil extracellular traps mediate the crosstalk between glioma progression and the tumor microenvironment via the HMGB1/RAGE/IL-8 axis显示文摘Objective:Neutrophil extracellular traps(NETs)produced by tumor-infiltrating neutrophils(TINs)are associated with poor prognosis in patients with several types of cancer.However,the mechanisms underlying the involvement of NETs in glioma progression remain largely unknown.This study aimed to elucidate the roles of NETs in biological processes that drive the crosstalk between glioma progression and the tumor microenvironment.Methods:Neutrophil infiltration and NETs formation were investigated in glioma tissue through immunohistochemistry,and their relationships with clinicopathological features and outcomes were statistically evaluated.The effects of NETs on glioma cell progression were studied in a co-culture system.In vivo and in vitro experiments validated the reactive oxygen species activity and cytokine production of TINs,as well as the ERK signaling pathway activation and the metastasis of gliomas.Results:Neutrophil infiltration and NETs formation were induced in high-grade glioma compared with low-grade glioma.NETs induced by TINs were determined to be an oncogenic marker of high-grade gliomas and to be involved in cell proliferation and invasion.NETs overproduction promoted glioma cell proliferation,migration,and invasion.Furthermore,HMGB1 was found to bind to RAGE and activate the NF-κB signaling pathway in vitro.In addition,NETs stimulated the NF-κB signaling pathway,thus promoting IL-8 secretion in glioblastoma.Subsequently,IL-8 recruited neutrophils which in turn mediated NETs formation via the PI3 K/AKT/ROS axis in TINs.Conclusions:Our results suggest that NETs produced by TINs mediate the crosstalk between glioma progression and the tumor microenvironment by regulating the HMGB1/RAGE/IL-8 axis.Targeting NETs formation or IL-8 secretion may be an effective approach to inhibit glioma progression. | Caijun Zha Xiangqi Meng Lulu Li Shan Mi Da Qian Ziwei Li Pengfei Wu Shaoshan Hu Shihong Zhao Jinquan Cai Yanhong Liu | 2020 | Cancer Biology & Medicine2020，17，1： | 19 |
| 2 | Anti-β2GPI/β2GPI complexes induce platelet activation and promote thrombosis via p38MAPK: a pathway to targeted therapies显示文摘Anti-β2 glycoprotein I(anti-β2GPI)antibodies are important contributors to the development of thrombosis.Anti-β2GPI antibody complexes withβ2GPI are well known to activate monocytes and endothelial cells via the intracellular NF-kB pathway with prothrombotic implications.By contrast,the interaction of anti-β2GPI/β2GPI complexes with platelets has not been extensively studied.The p38 mitogen-activated protein kinase(MAPK)pathway has been recognized to be an important intracellular signaling pathway in the coagulation cascade and an integral component of arterial and venous thrombosis.The present study reveals that levels of anti-β2GPI/β2GPI complexes in sera are positively associated with p38MAPK phosphorylation of platelets in thrombotic patients.Furthermore,SB203580 inhibits anti-β2GPI/β2GPI complex-induced platelet activation.Thrombus formation decreased in p38MAPK−/−mice after treatment with anti-β2GPI/β2GPI complexes.In conclusion,p38MAPK may be a treatment target for anti-β2GPI antibody-associated thrombotic events. | Wenjing Zhang Caijun Zha Xiumin Lu Ruichun Jia Fei Gao Qi Sun Meili Jin Yanhong Li | 2019 | Frontiers of Medicine2019，13，6： | 3 |
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