24 results on '"Jun-tang Li"'
Search Results
2. Anesthetic Isoflurane Posttreatment Attenuates Experimental Lung Injury by Inhibiting Inflammation and Apoptosis
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Jun-tang Li, Hui Wang, Wei Li, Li-feng Wang, Li-chao Hou, Jing-lan Mu, Xin Liu, Hui-juan Chen, Ke-lang Xie, Nan-lin Li, and Chun-fang Gao
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Pathology ,RB1-214 - Abstract
We investigated the effect of 1.4% isoflurane (ISO) on the development of inflammation and apoptosis caused by zymosan (ZY) in mice. We found that ZY-challenged mice exhibited significant body weight loss, markedly high mortality, and significant lung injury characterized by the deterioration of histopathology, histologic scores, and wet-to-dry ratio after ISO treatment. ISO dramatically attenuated ZY-induced lung neutrophil recruitment and inflammation, as evidenced by the reduced levels of total cells, neutrophils, and proinflammatory cytokines (i.e., tumor necrosis factor-α, interleukin- (IL-) 1β, IL-6, and macrophage inflammatory protein-2) in bronchoalveolar lavage fluid and of their mRNA expression in lung tissues. ISO also inhibited ZY-induced expression and activation of nuclear factor-kappaB p65 and inducible nitric oxide synthase in pulmonary tissue. ZY administration also resulted in the upregulation of heme oxygenase-1 expression and activity in the lung, which was further enhanced by ISO treatment. Moreover, ISO markedly prevented ZY-induced pulmonary cell apoptosis in mice, as reflected by the decrease in expression of procaspase-8, procaspase-3, cleaved caspase-8, and cleaved caspase-3, as well as in caspase-3 activity and Bcl-2-associated X/B-cell lymphoma 2 ratio. These results indicate that ISO is a potential therapeutic drug for treating ZY-induced lung injury, and further investigations are warranted.
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- 2013
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3. A Subanesthetic Dose of Isoflurane during Postconditioning Ameliorates Zymosan-Induced Neutrophil Inflammation Lung Injury and Mortality in Mice
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Hui Wang, Jing Fan, Nan-lin Li, Jun-tang Li, Shi-fang Yuan, Jun Yi, Ling Wang, Jiang-hao Chen, Yong-gang Lv, Qing Yao, Ting Wang, Yu-cai Wang, and Rui Ling
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Pathology ,RB1-214 - Abstract
Anesthetic isoflurane (ISO) has immunomodulatory effects. In the present study, we investigated whether a subanesthetic dose of ISO (0.7%) protected against zymosan (ZY) induced inflammatory responses in the murine lung and isolated neutrophils. At 1 and 6 hrs after ZY administration intraperitoneally, ISO was inhaled for 1 hr, and 24 hrs later, lung inflammation and injury were assessed. We found that ISO improved the survival rate of mice and mitigated lung injury as characterized by the histopathology, wet-to-dry weight ratio, protein leakage, and lung function index. ISO significantly attenuated ZY-induced lung neutrophil recruitment and inflammation. This was suggested by the downregulation of (a) endothelial adhesion molecule expression and myeloperoxidase (MPO) activity in lung tissue and polymorphonuclear neutrophils (b) chemokines, and (c) proinflammatory cytokines in BALF. Furthermore, ZY-induced nuclear translocation and DNA-binding activity of NF-κB p65 were also reduced by ISO. ISO treatment inhibited iNOS expression and activity, as well as subsequent nitric oxide generation. Consistent with these in vivo observations, in vitro studies confirmed that ISO blocked NF-κB and iNOS activation in primary mouse neutrophils challenged by ZY. These results provide evidence that 0.7% ISO ameliorates inflammatory responses in ZY-treated mouse lung and primary neutrophils.
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- 2013
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4. Ectopically expressed perforin-1 is proapoptotic in tumor cell lines by increasing caspase-3 activity and the nuclear translocation of cytochrome C.
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Li-Feng Wang, Fang Wang, Jun-Tang Li, Wei-Hong Wen, Jing Zhao, Lin-Tao Jia, Yan-Ling Meng, Yun-Xin Cao, Li-Bo Yao, Si-Yi Chen, Yan-Ming Xu, and An-Gang Yang
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Medicine ,Science - Abstract
Perforin-1 (PRF), a cytotoxic lymphocyte pore-forming protein, plays an important role in the action of cytotoxic T cells and natural killer cells in that it causes the lysis of abnormal body cells and the elimination of virus-infected cells and tumors. Upon degranulation, PRF inserts itself into the target cell's plasma membrane, forming a pore. The subsequent translocation of pro-apoptotic granzymes (including granzyme B, A, M et al.) into the cytoplasm provides the proteases with access to numerous protein substrates that promote apoptosis after cleavage. These proteases are believed to be the main executioners of target cell apoptosis. Although the PRF and granzyme components are both critical to this process and in some way involved in inducing cell death in target cells, the inhibition of tumor growth could still be efficient in granzyme-deficient mice. It is unclear whether PRF alone can suppress tumors. In this study, we discovered that forced ectopic expression of PRF alone, in the absence of granzymes, could mediate cell death in cancer cells. Notably, transient expression of both full-length and truncated active-form PRF in human Hep G2, SK-BR-3, and HeLa cells was found to induce apparent cell growth inhibition and cell death, as evidenced by chromosome condensation and DNA fragmentation, increased caspase-3 activity, and the release of apoptosis inducing factor (AIF) and cytochrome c from the mitochondria. This PRF-induced cell death could be abrogated by pan-caspase inhibitor (Z-VAD) and mitochondria protector (TAT-BH4). The implication of these results is that ectopically expressed PRF has apoptosis-inducing abilities, and PRF alone is sufficient to induce apoptotic cell death in cells with ectopic expression. Taking this into consideration, our results suggest the possibility of using PRF as a pro-apoptotic gene for tumor therapeutics.
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- 2012
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5. Subanesthetic isoflurane abates ROS-activated MAPK/NF-κB signaling to repress ischemia-induced microglia inflammation and brain injury
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Jun-Tang Li, Xiao-Shan Zhu, Ya-Li Zhao, Ling Wang, Ning-Ning Liu, Zhiqiang Yao, Qin-Qin Liu, and Chun-Fang Gao
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MAPK/ERK pathway ,Aging ,p38 mitogen-activated protein kinases ,Interleukin-1beta ,Ischemia ,microglia ,Nitric Oxide Synthase Type II ,Apoptosis ,Inflammation ,ischemia ,Pharmacology ,p38 Mitogen-Activated Protein Kinases ,Brain Ischemia ,isoflurane ,medicine ,Animals ,Chemokine CCL2 ,Neurons ,Microglia ,Interleukin-6 ,Tumor Necrosis Factor-alpha ,Chemistry ,Interleukin-8 ,NF-kappa B ,ROS ,Infarction, Middle Cerebral Artery ,Cell Biology ,medicine.disease ,neuron ,Coculture Techniques ,Rats ,carbohydrates (lipids) ,Disease Models, Animal ,medicine.anatomical_structure ,nervous system ,Cyclooxygenase 2 ,Anesthetics, Inhalation ,Tumor necrosis factor alpha ,Neuron ,medicine.symptom ,Reactive Oxygen Species ,Research Paper - Abstract
Isoflurane (ISO) elicits protective effects on ischemia-induced brain injury. We investigated whether sub-anesthetic (0.7%) ISO post-conditioning attenuates the inflammation and apoptosis in oxygen-glucose deprivation (OGD)-insulted co-cultures (microglia and neurons) in vitro and the brain injury of the middle cerebral arterial occlusion (MCAO) rat. We demonstrated that ISO augmented the viability of OGD-treated microglia and neurons. ISO reduced the expression and activation of COX2 and iNOS in OGD-challenged microglia. ISO repressed the production of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, IL-8, and monocyte chemoattractant protein-1 in OGD-exposed microglia. ISO also decreased nucleosomal fragmentation and caspase-3 activity but increased mitochondrial membrane potential in OGD-stimulated microglia and neurons. Mechanistically, ISO suppressed OGD-induced microglial inflammation by blocking ROS-regulated p38 MAPK/NF-κB signaling pathway and hampered OGD-triggered microglial apoptosis in a ROS- or NO-dependent fashion. In vivo results with MCAO rats were partly consistent with the in vitro observation. These findings indicate that sub-anesthetic ISO post-conditioning abates the inflammation and apoptosis in OGD-stimulated rat microglia and the apoptosis of OGD-exposed neurons and the brain injuries of MCAO rats, suggesting it as a potentially effective therapeutic approach for ischemic brain damages.
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- 2020
6. Oncogenic USP22 supports gastric cancer growth and metastasis by activating c-Myc/NAMPT/SIRT1-dependent FOXO1 and YAP signaling
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Qin-Qin Liu, Xiao-Shan Zhu, Ya-Li Zhao, Jun-Tang Li, Hongxia Liu, Chun-Fang Gao, Xusheng Zhao, Ning-Ning Liu, and Changsong Wang
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Male ,Aging ,proliferation ,FOXO1 ,Apoptosis ,Mice, SCID ,Metastasis ,Proto-Oncogene Proteins c-myc ,Mice ,Western blot ,Sirtuin 1 ,Cell Movement ,Stomach Neoplasms ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Neoplasm Invasiveness ,Nicotinamide Phosphoribosyltransferase ,Adaptor Proteins, Signal Transducing ,Aged ,Cell Proliferation ,Gene knockdown ,medicine.diagnostic_test ,Chemistry ,Forkhead Box Protein O1 ,gastric cancer ,Cancer ,YAP-Signaling Proteins ,Cell Biology ,Middle Aged ,medicine.disease ,invasion ,Prognosis ,Cell culture ,Gene Knockdown Techniques ,ubiquitin-specific peptidase 22 ,Cancer research ,Cytokines ,Female ,Signal transduction ,Ubiquitin Thiolesterase ,Research Paper ,Signal Transduction ,Transcription Factors - Abstract
In this study, we investigated the role of ubiquitin-specific protease 22 (USP22) in the growth and progression of gastric cancer (GC). USP22 mRNA and protein levels were significantly higher in GC tissue samples and GC cell lines than in adjacent noncancerous tissue samples and a normal gastric mucosal epithelial cell line (GES1), respectively. USP22 knockdown significantly decreased in vitro survival, proliferation, migration, and invasiveness of GC cells compared with the controls. Western blot analysis of control and USP22-silenced GC cells showed that USP22 modulates the c-Myc/NAMPT/SIRT1-dependent FOXO1 and YAP signaling pathways. Subcutanenous injection of USP22-silenced GC cells into SCID mice generated significantly smaller xenograft tumors than did control cells. Moreover, USP22-silenced GC cells showed less lung metastasis than the controls following tail vein injection in SCID mice. In addition, high USP22 expression correlated positively with tumor size, advanced stage and metastasis, and correlated negatively with tumor differentiation and prognosis in GC patients. These results show that USP22 regulates growth and progression of GC via the c-Myc/NAMPT/SIRT1-dependent FOXO1 and YAP signaling pathways.
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- 2019
7. Exploring transgene transfer from the transgenic chicken model to its offspring through a nonviral vector
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Ming Yan Shi, Ting Sheng Xu, Zhen Hong Li, Xue Qin Lei, Guang Hui Wei, Pan Lin Wang, Jun Tang Li, Guang Ping Zhang, and Zhen Song
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0301 basic medicine ,animal structures ,030102 biochemistry & molecular biology ,Offspring ,Transgene ,Organic Chemistry ,Transfection ,Biology ,Biochemistry ,Molecular biology ,Marker gene ,Green fluorescent protein ,03 medical and health sciences ,030104 developmental biology ,embryonic structures ,Scaffold/matrix attachment region ,Gene ,Blastoderm - Abstract
There is much interest in using chickens as “bioreactors” to produce large quantities of biopharmaceuticals. However, transient expression of foreign genes have been known to cause low efficiency of obtaining transgenic offspring, especially when using nonviral vectors. In present study, a transgenic chicken model was investigated to determine whether an exogenous gene can be expressed stably and transferred to its offspring through a matrix attachment region (MAR)-mediated non-viral vector using the eGFP marker gene. The eukaryotic expression vector pEGFP-N1-MAR, which contains the eGFP gene and MAR, was constructed and transfected into a chicken stage-X blastoderm to produce a G0 generation of transgenic chickens. The hatchabilities of different injection regions were tested; 18 of the 40 eggs injected with pEGFPN1- MAR in the area opaca hatched after 21 days of incubation, and had a hatchability rate of 45%. By contrast, eggs injected at the area pellucida did not hatch. Results from the fluorescence signal detection and polymerase chain reaction (PCR) verified that four hatched chicks from the G0 generation expressed the eGFP gene. Furthermore, fluorescence signal detection results indicated that 2 of the 65 chicks from the G1 generation expressed the eGFP gene. We conclude that MAR facilitates the production of transgenic chickens; pEGFP-N1-MAR application is a novel approach that can produce transgenic chicken offspring.
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- 2017
8. Swimming attenuates inflammation, oxidative stress, and apoptosis in a rat model of dextran sulfate sodium-induced chronic colitis
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Jun-Tang Li, Lifeng Wang, Ya-Li Zhao, Ning-Ning Liu, Zhiqiang Yao, Xiao-Shan Zhu, Ling Qin, Angang Yang, Chun-Fang Gao, Qi Chang, and Qin-Qin Liu
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Male ,0301 basic medicine ,Time Factors ,CD3 Complex ,T-Lymphocytes ,medicine.medical_treatment ,Apoptosis ,Pharmacology ,Weight Gain ,medicine.disease_cause ,Antioxidants ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,oxidative stress ,swimming ,chemistry.chemical_classification ,biology ,Glutathione peroxidase ,Dextran Sulfate ,Research Paper: Immunology ,Colitis ,Malondialdehyde ,Exercise Therapy ,Cytokine ,Neutrophil Infiltration ,Oncology ,Immunology and Microbiology Section ,Inflammation Mediators ,medicine.symptom ,Signal Transduction ,Colon ,Inflammation ,Superoxide dismutase ,03 medical and health sciences ,medicine ,Animals ,Immune response ,business.industry ,Immunity ,chronic colitis ,medicine.disease ,Disease Models, Animal ,030104 developmental biology ,chemistry ,inflammation ,Chronic Disease ,Splenomegaly ,Immunology ,biology.protein ,Calprotectin ,Apoptosis Regulatory Proteins ,Reactive Oxygen Species ,business ,Biomarkers ,Oxidative stress - Abstract
// Ling Qin 1,* , Zhi-qiang Yao 2,* , Qi Chang 3,* , Ya-li Zhao 2,* , Ning-ning Liu 2,* , Xiao-shan Zhu 2 , Qin-qin Liu 2 , Li-feng Wang 4 , An-gang Yang 5 , Chun-fang Gao 2 and Jun-tang Li 2,3,4,5 1 Department of Hematology, First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, Henan, China 2 Centre of Inflammation and Cancer Research, 150th Central Hospital of PLA, Luoyang, Henan, China 3 Centre of Biomaterial and Biophysics Research, Institute of Training Medicine, 150th Central Hospital of PLA, Luoyang, Henan, China 4 State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi’an, Shaanxi, China 5 State Key Laboratory of Cancer Biology, Department of Immunology, Fourth Military Medical University, Xi’an, Shaanxi, China * These authors have contributed equally to this work Correspondence to: Jun-tang Li, email: // Chun-fang Gao, email: // Ling Qin, email: // Keywords : chronic colitis, swimming, inflammation, oxidative stress, apoptosis, Immunology and Microbiology Section, Immune response, Immunity Received : March 28, 2016 Accepted : December 15, 2016 Published : December 21, 2016 Abstract Increasing evidence suggests that regular physical exercise suppresses chronic inflammation. However, the potential inhibitory effects of swimming on dextran sulfate sodium (DSS)-induced chronic colitis, and its underlying mechanisms, remain unclear. In this study, rats were orally administered DSS to induce chronic colitis, and subsequently treated with or without swimming exercise. A 7-week swimming program (1 or 1.5 hours per day, 5 days per week) ameliorated DSS-caused colon shortening, colon barrier disruption, spleen enlargement, serum LDH release, and reduction of body weight gain. Swimming for 1.5 hours per day afforded greater protection than 1 hour per day. Swimming ameliorated DSS-induced decrease in crypt depth, and increases in myeloperoxidase activity, infiltration of Ly6G + neutrophils and TNF-α- and IFN-γ-expressing CD3 + T cells, as well as fecal calprotectin and lactoferrin. Swimming inhibited pro-inflammatory cytokine and chemokine production and decreased the protein expression of phosphorylated nuclear factor-κB p65 and cyclooxygenase 2, whereas it elevated interleukin-10 levels. Swimming impeded the generation of reactive oxygen species, malondialdehyde, and nitric oxide; however, it boosted glutathione levels, total antioxidant capacity, and superoxide dismutase and glutathione peroxidase activities. Additionally, swimming decreased caspase-3 activity and expression of apoptosis-inducing factor, cytochrome c, Bax, and cleaved-caspase-3, but increased Bcl-2 levels. Overall, these results suggest that swimming exerts beneficial effects on DSS-induced chronic colitis by modulating inflammation, oxidative stress, and apoptosis.
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- 2016
9. Targeting ubiquitin-specific protease 22 suppresses growth and metastasis of anaplastic thyroid carcinoma
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Jun-Tang Li, Qin-Qin Liu, Xiao-Shan Zhu, Hai-Li Tang, Chun-Fang Gao, Ya-Li Zhao, Ning-Ning Liu, Angang Yang, Lin-Tao Jia, and Hua-Dong Zhao
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0301 basic medicine ,proliferation ,Down-Regulation ,Mice, SCID ,Thyroid Carcinoma, Anaplastic ,Metastasis ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Cyclin D2 ,Downregulation and upregulation ,Cell Line, Tumor ,Gene silencing ,Medicine ,Animals ,Humans ,ubiquitin-specific protease 22 ,Thyroid Neoplasms ,Neoplasm Metastasis ,Protein kinase B ,Gene knockdown ,business.industry ,anaplastic thyroid carcinoma ,apoptosis ,Cell migration ,medicine.disease ,invasion ,Prognosis ,030104 developmental biology ,Oncology ,030220 oncology & carcinogenesis ,Gene Knockdown Techniques ,Immunology ,Cancer research ,Heterografts ,Female ,Thiolester Hydrolases ,Signal transduction ,business ,Ubiquitin Thiolesterase ,Research Paper ,Signal Transduction - Abstract
Ubiquitin-specific protease 22 (USP22) aberrance has been implicated in several malignancies; however, whether USP22 plays a role in anaplastic thyroid carcinoma (ATC) remains unclear. Here, we report that USP22 expression is highly elevated in ATC tissues, which positively correlated with tumor size, extracapsular invasion, clinical stages, and poor prognosis of ATC patients. In vitro assays showed that USP22 depletion suppressed ATC cell survival and proliferation by decreasing Rb phosphorylation and cyclin D2, inactivating Akt, and simultaneously upregulating Rb; USP22 silencing restrained cell migration and invasion by inhibiting epithelial-mesenchymal transition; USP22 knockdown promoted mitochondrion- mediated and caspase-dependent apoptosis by upregulating Bax and Bid and promoting caspase-3 activation. Consistent with in vitro findings, downregulation of USP22 in ATC cells impeded tumor growth and lung metastasis in vivo. These results raise the applicability for USP22 as a useful predictor of ATC prognosis and a potential therapeutic target for ATC.
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- 2016
10. Subanesthetic isoflurane relieves zymosan-induced neutrophil inflammatory response by targeting NMDA glutamate receptor and Toll-like receptor 2 signaling
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Ya-Li Zhao, Qin-Qin Liu, Angang Yang, Xiao-Shan Zhu, Jun-Tang Li, Chun-Fang Gao, Wei-Qi Wang, Lin-Tao Jia, Ling Wang, and Ning-Ning Liu
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0301 basic medicine ,Time Factors ,Neutrophils ,Anti-Inflammatory Agents ,Nitric Oxide Synthase Type II ,p38 Mitogen-Activated Protein Kinases ,chemistry.chemical_compound ,Mice ,Medicine ,TLR2 ,Receptor ,Lung ,Cells, Cultured ,Toll-like receptor ,NADPH oxidase ,biology ,Research Paper: Immunology ,NF-kappa B ,neutrophil ,src-Family Kinases ,Oncology ,Immunology and Microbiology Section ,RNA Interference ,medicine.symptom ,Signal transduction ,Signal Transduction ,Acute Lung Injury ,Inflammation ,Nerve Tissue Proteins ,Lung injury ,Nitric Oxide ,Transfection ,Receptors, N-Methyl-D-Aspartate ,zymosan ,Capillary Permeability ,03 medical and health sciences ,isoflurane ,Peroxynitrous Acid ,Animals ,Immune response ,030102 biochemistry & molecular biology ,Dose-Response Relationship, Drug ,business.industry ,Zymosan ,Immunity ,Endothelial Cells ,Pneumonia ,NMDA receptor ,Toll-Like Receptor 2 ,Disease Models, Animal ,030104 developmental biology ,chemistry ,Immunology ,biology.protein ,business - Abstract
// Jun-Tang Li 1,2,3,* , Wei-Qi Wang 4,5,6,* , Ling Wang 7,* , Ning-Ning Liu 1,* , Ya-Li Zhao 1,* , Xiao-Shan Zhu 1 , Qin-Qin Liu 1 , Chun-Fang Gao 1 , An-Gang Yang 2 and Lin-Tao Jia 3 1 Centre of Inflammation and Cancer Research, 150th Central Hospital of PLA, Luoyang, Henan, China 2 State Key Laboratory of Cancer Biology, Department of Immunology, Fourth Military Medical University, Xi’an, Shaanxi, China 3 State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi’an, Shaanxi, China 4 State Key Laboratory of Military Stomatology, Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi’an, China 5 National Clinical Research Center for Oral Diseases, Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi’an, China 6 Shaanxi Clinical Research Center for Oral Diseases, Department of Oral and Maxillofacial Surgery, School of Stomatology, Fourth Military Medical University, Xi’an, China 7 Department of Anesthesiology, 150th Central Hospital of PLA, Luoyang, Henan, China * These authors have contributed equally to this work Correspondence to: Jun-Tang Li, email: // An-Gang Yang, email: // Lin-Tao Jia, email: // Keywords : isoflurane, zymosan, neutrophil, NMDA receptor, TLR2, Immunology and Microbiology Section, Immune response, Immunity Received : September 07, 2015 Accepted : April 18, 2016 Published : April 28, 2016 Abstract Neutrophil release of NO/ONOO – induces endothelial cell barrier dysfunction in inflammatory acute lung injury (ALI). Previous studies using zymosan-triggered inflammation and ALI model revealed that zymosan promotes inducible NO synthase (iNOS) expression in neutrophils, and that isoflurane inhibits zymosan-induced oxidative stress and iNOS biosynthesis. However, the underlying mechanisms remain largely unknown. We found here that in zymosan-primed neutrophils, iNOS is transcriptionally activated by NF-κB, whose nuclear translocation is triggered by excessive reactive oxygen species (ROS) and consequently activated p38 MAPK. ROS production is attributed to zymosan-initiated Toll-like receptor 2 (TLR2) signaling, in which the adaptor MyD88 recruits and activates c-Src, and c-Src activates NADPH oxidase to generate ROS. Subanesthetic isoflurane counteracts the aforementioned zymosan-induced signaling by targeting N-methyl-D-aspartic acid (NMDA) glutamate receptor and thereby suppressing calcium influx and c-Src activation. Whereas iNOS accelerates NO/ONOO – production in neutrophils which eventually promote protein leak from pulmonary microvascular endothelial cells (PMVEC), isoflurane reduced NO/ONOO – release from zymosan-treated neutrophils, and thus relieves trans-PMVEC protein leak. This study provides novel insights into the roles of neutrophils and the underlying mechanisms in zymosan-induced ALI, and has implications for the therapeutic potential of subanesthetic isoflurane in attenuating inflammatory responses causing lung endothelial cell damage.
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- 2016
11. Integrative bioinformatics and proteomics-based discovery of an eEF2K inhibitor (cefatrizine) with ER stress modulation in breast cancer cells
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Liu Yigang, Nan Jia, Lu Zheng, Jun-Tang Li, Xiao-Shan Zhu, Jiangbo Du, Nai-Jun Fan, Ci Lv, Ying Zhang, Wang Xingke, Feng Xie, Chun-Fang Gao, Ning-Ning Liu, Zhiqiang Yao, Zhou Fei, Liu Zhongyu, and Jing-Jing Lv
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Elongation Factor 2 Kinase ,Proteomics ,0301 basic medicine ,Breast Neoplasms ,Context (language use) ,Biology ,Bioinformatics ,03 medical and health sciences ,Cell Line, Tumor ,medicine ,Humans ,Protein kinase A ,Protein Kinase Inhibitors ,Molecular Biology ,Cell Proliferation ,Integrative bioinformatics ,Kinase ,Cefatrizine ,Computational Biology ,Cancer ,Endoplasmic Reticulum Stress ,medicine.disease ,030104 developmental biology ,Cancer research ,Unfolded protein response ,Female ,Biotechnology ,medicine.drug - Abstract
Eukaryotic elongation factor-2 kinase (eEF2K), a unique calcium/calmodulin-dependent protein kinase, is well known to regulate apoptosis, autophagy and ER stress in many types of human cancers. Therefore, eEF2K would be regarded as a promising therapeutic target; however, the eEF2K-regulated mechanism and its targeted inhibitor still remain to be discovered in cancer. Herein, we constructed a protein-protein interaction (PPI) network of eEF2K and achieved an eEF2K-regulated ER stress subnetwork by bioinformatics prediction. Then, we found that the differential protein expressions involved in ER stress in the context of si-eEF2K-treated MCF-7 and MDA-MB-436 cells by iTRAQ-based analyses, respectively. Integrated into these aforementioned results, we constructed a core eEF2K-regulated ER stress subnetwork in breast cancer cells. Subsequently, we screened a series of candidate compounds targeting eEF2K and discovered a novel eEF2K inhibitor (cefatrizine) with an anti-proliferative activity toward breast cancer cells. Moreover, we found that cefatrizine induced ER stress in both MCF-7 and MDA-MB-436 cells. Interestingly, we demonstrated that the mechanism of cefatrizine-induced ER stress was in good agreement with our bioinformatics and proteomics-based results. In conclusion, these results demonstrate that a novel eEF2K inhibitor (cefatrizine) induces ER stress in breast cancer cells by integrating bioinformatics prediction, proteomics analyses and experimental validation, which would provide a clue for exploring more mechanisms of eEF2K and its targeted inhibitors in cancer therapy.
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- 2016
12. MiRNA-101 inhibits breast cancer growth and metastasis by targeting CX chemokine receptor 7
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Qin-Qin Liu, Angang Yang, Jun-Tang Li, Chun-Fang Gao, Ning-Ning Liu, Xiu-Li Wang, Lin-Tao Jia, Yan-Li Liu, Xiao-Shan Zhu, and Feng Yu
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STAT3 Transcription Factor ,Pathology ,medicine.medical_specialty ,Lung Neoplasms ,Time Factors ,MiR-101 ,proliferation ,Apoptosis ,Breast Neoplasms ,Kaplan-Meier Estimate ,Transfection ,Metastasis ,Chemokine receptor ,breast cancer ,Breast cancer ,Cell Movement ,In vivo ,Cell Line, Tumor ,microRNA ,medicine ,metastasis ,Animals ,Humans ,Neoplasm Invasiveness ,skin and connective tissue diseases ,Cell Proliferation ,Receptors, CXCR ,Mice, Inbred BALB C ,business.industry ,Cell growth ,medicine.disease ,CXCR7 ,Tumor Burden ,Gene Expression Regulation, Neoplastic ,MicroRNAs ,HEK293 Cells ,Oncology ,Lymphatic Metastasis ,Cancer research ,Female ,RNA Interference ,Neoplasm Grading ,Signal transduction ,business ,Research Paper ,Signal Transduction - Abstract
Whereas miR-101 is involved in the development and progression of breast cancer, the underlying molecular mechanisms remain to be elucidated. Here, we report that miR-101 expression is inversely correlated with the clinical stage, lymph node metastasis and prognosis in breast cancers. Introduction of miR-101 inhibited breast cancer cell proliferation and invasion in vitro and suppressed tumor growth and lung metastasis of in vivo. CX chemokine receptor 7 (CXCR7) is a direct target of miR-101, positively correlating with the histological grade and the incidence of lymph node metastasis in breast cancer patients. The effects of miR-101 were mimicked and counteracted by CXCR7 depletion and overexpression, respectively. STAT3 signaling downstream of CXCR7 is involved in miR-101 regulation of breast cancer cell behaviors. These findings have implications for the potential application of miR-101 in breast cancer treatment.
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- 2015
13. Identification of tubulin beta chain, thymosin beta-4-like protein 3, and cytochrome b–c1 complex subunit 1 as serological diagnostic biomarkers of gastric cancer
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Chun-Fang Gao, Liang Hu, Xiu-Li Wang, Qing-Yin Liu, Ke Li, Jun-Tang Li, and Nai-Jun Fan
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chemistry.chemical_classification ,Cytochrome ,biology ,Tubulin Beta Chain ,Cytochrome b ,Protein subunit ,Clinical Biochemistry ,Thymosin ,Peptide ,General Medicine ,Proteomics ,Molecular biology ,Thymosin beta-4 ,chemistry ,biology.protein - Abstract
Objective Despite major advances in its diagnosis and treatment, gastric cancer (GC) remains a major life-threatening disease. Treatment of the disease is further aggravated by the lack of diagnostic biomarkers that can aid in the early detection of GC and promote its favorable prognosis. The present work aims to identify novel diagnostic biomarkers for GC. Design and methods The present work is a case–control study that focuses on proteomic analysis of serum from healthy volunteers and GC patients using ClinProt profiling technology based on mass spectrometry. A pattern of proteins/peptides with the ability to differentiate the studied populations was identified. Deregulated proteins/peptides differentially expressed in the serum of patients compared with healthy volunteers were identified by mass spectroscopy. Results A pattern of proteins/peptides consisting of four protein/peptide peaks at m/z 1467, 1867, 2701, and 2094 was identified. These protein/peptide peaks were able to differentiate the studied populations with close to 100% sensitivity and specificity. Three of the deregulated proteins/peptides at m/z 1867, 2701, and 2094 were identified by mass spectroscopy (LTQ Orbitrap XL) as tubulin beta chain, thymosin beta-4-like protein 3, and cytochrome b–c1 complex subunit 1, respectively. Conclusions The pattern of proteins/peptides identified in the present work shows great potential for GC diagnosis. Deregulated proteins of tubulin beta chain, thymosin beta-4-like protein 3, and cytochrome b–c1 complex subunit 1 may be involved in the pathogenesis of GC and serve as potential serological diagnostic biomarkers.
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- 2013
14. Anesthetic Isoflurane Posttreatment Attenuates Experimental Lung Injury by Inhibiting Inflammation and Apoptosis
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Hui-Hui Wang, Ke-lang Xie, Jun-Tang Li, Wei Li, Jinglan Mu, Huijuan Chen, Nanlin Li, Li-chao Hou, Chunfang Gao, Xin Liu, and Li-Feng Wang
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Male ,Pathology ,medicine.medical_specialty ,Article Subject ,Blotting, Western ,Interleukin-1beta ,Immunology ,Apoptosis ,Enzyme-Linked Immunosorbent Assay ,Inflammation ,Pharmacology ,Biology ,Lung injury ,Proinflammatory cytokine ,Mice ,chemistry.chemical_compound ,lcsh:Pathology ,medicine ,Animals ,Mice, Inbred BALB C ,Isoflurane ,medicine.diagnostic_test ,Interleukin-6 ,Reverse Transcriptase Polymerase Chain Reaction ,Tumor Necrosis Factor-alpha ,Zymosan ,Interleukin ,Lung Injury ,Cell Biology ,Immunohistochemistry ,Nitric oxide synthase ,Bronchoalveolar lavage ,Neutrophil Infiltration ,chemistry ,Anesthetics, Inhalation ,biology.protein ,Tumor necrosis factor alpha ,medicine.symptom ,lcsh:RB1-214 ,Research Article - Abstract
We investigated the effect of 1.4% isoflurane (ISO) on the development of inflammation and apoptosis caused by zymosan (ZY) in mice. We found that ZY-challenged mice exhibited significant body weight loss, markedly high mortality, and significant lung injury characterized by the deterioration of histopathology, histologic scores, and wet-to-dry ratio after ISO treatment. ISO dramatically attenuated ZY-induced lung neutrophil recruitment and inflammation, as evidenced by the reduced levels of total cells, neutrophils, and proinflammatory cytokines (i.e., tumor necrosis factor-α, interleukin- (IL-) 1β, IL-6, and macrophage inflammatory protein-2) in bronchoalveolar lavage fluid and of their mRNA expression in lung tissues. ISO also inhibited ZY-induced expression and activation of nuclear factor-kappaB p65 and inducible nitric oxide synthase in pulmonary tissue. ZY administration also resulted in the upregulation of heme oxygenase-1 expression and activity in the lung, which was further enhanced by ISO treatment. Moreover, ISO markedly prevented ZY-induced pulmonary cell apoptosis in mice, as reflected by the decrease in expression of procaspase-8, procaspase-3, cleaved caspase-8, and cleaved caspase-3, as well as in caspase-3 activity and Bcl-2-associated X/B-cell lymphoma 2 ratio. These results indicate that ISO is a potential therapeutic drug for treating ZY-induced lung injury, and further investigations are warranted.
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- 2013
15. RETRACTED ARTICLE: Nuclear factor of activated T cells 5 maintained by Hotair suppression of miR-568 upregulates S100 calcium binding protein A4 to promote breast cancer metastasis
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Lei Wang, Chunfang Gao, Jing Zhao, Jun-Tang Li, Wei Li, Ya-Li Zhao, Yan-Ling Meng, Lin-Tao Jia, Ning-Ning Liu, Angang Yang, Tao Yang, Lifeng Wang, Xiao-Shan Zhu, and Feng Yu
- Subjects
Medicine(all) ,Regulation of gene expression ,business.industry ,Angiogenesis ,HOTAIR ,medicine.disease ,Bioinformatics ,Metastasis ,Breast cancer ,microRNA ,medicine ,Cancer research ,Gene silencing ,Epithelial–mesenchymal transition ,business ,Research Article - Abstract
Introduction The onset of distal metastasis, which underlies the high mortality of breast cancers, warrants substantial studies to depict its molecular basis. Nuclear factor of activated T cells 5 (NFAT5) is upregulated in various malignancies and is critically involved in migration and invasion of neoplastic cells. Nevertheless, the metastasis-related events potentiated by this transcriptional factor and the mechanism responsible for NFAT5 elevation in carcinoma cells remain to be fully elucidated. Methods The correlation of NFAT5 with breast cancer invasiveness was investigated in vitro and clinically. The genes transcriptionally activated by NFAT5 were probed and their roles in breast cancer progression were dissected. The upstream regulators of NFAT5 were studied with particular attempt to explore the involvement of non-coding RNAs, and the mechanism underlying the maintenance of NFAT5 expression was deciphered. Results In metastatic breast cancers, NFAT5 promotes epithelial-mesenchymal transition (EMT) and invasion of cells by switching on the expression of the calcium binding protein S100A4, and facilitates the angiogenesis of breast epithelial cells and thus the development of metastases by transcriptionally activating vascular endothelial growth factor C (VEGF-C). NFAT5 is directly targeted by miR-568, which is in turn suppressed by the long non-coding RNA, Hotair, via a documented in trans gene silencing pattern, that is recruitment of the polycomb complex (Polycomb Repressive Complex 2; PRC2) and LSD1, and consequently methylation of histone H3K27 and demethylation of H3K4 on the miR-568 loci. Conclusion This study unravels a detailed role of NFAT5 in mediating metastatic signaling, and provides broad insights into the involvement of Hotair, in particular, by transcriptionally regulating the expression of microRNA(s), in the metastasis of breast cancers. Electronic supplementary material The online version of this article (doi:10.1186/s13058-014-0454-2) contains supplementary material, which is available to authorized users.
- Published
- 2014
16. Exploring Transgene Transfer From The Transgenic Chicken Model To Its Offspring through A Nonviral Vector, 'Биоорганическая химия'
- Author
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Lin Wang Pan, Ming Yan Shi, Zhen Song, Jun Tang Li, Zhen Hong Li, Ting Sheng Xu, Guang Ping Zhang, Guang Hui Wei, and Xue Qin Lei
- Subjects
Offspring ,Transgene ,General Medicine ,Vector (molecular biology) ,Biology ,Cell biology - Published
- 2017
17. MiR-568 inhibits the activation and function of CD4⁺ T cells and Treg cells by targeting NFAT5
- Author
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Angang Yang, Bo-Quan Jin, Weihong Wen, Yan-Ling Meng, Zhangyan Guo, Jun-Tang Li, Qian Xue, Wei Li, Lingbo Kong, and Tao Yang
- Subjects
CD4-Positive T-Lymphocytes ,Immunology ,Blotting, Western ,Gene Expression ,Biology ,Lymphocyte Activation ,Jurkat cells ,T-Lymphocytes, Regulatory ,Interleukin 21 ,Jurkat Cells ,Immunology and Allergy ,Cytotoxic T cell ,Humans ,IL-2 receptor ,CD154 ,Antigen-presenting cell ,Luciferases ,3' Untranslated Regions ,Cells, Cultured ,Cell Proliferation ,Reverse Transcriptase Polymerase Chain Reaction ,ZAP70 ,Cell Differentiation ,General Medicine ,Natural killer T cell ,Flow Cytometry ,Molecular biology ,Cell biology ,MicroRNAs ,HEK293 Cells ,Mutation ,Interleukin-2 ,RNA Interference ,Transcription Factors - Abstract
CD4+ T cells play critical roles in orchestrating adaptive immune responses. Their activation and proliferation are critical steps that occur before they execute their biological functions. Despite the important role of this process, the underlying molecular events are not fully understood. MicroRNAs (miRNAs) have been shown to play important roles in lymphocyte development and function. However, the miRNAs that regulate T-cell differentiation, activation and proliferation are still largely unknown. In our previous study, using a miRNA array, we found that several miRNAs (including miR-202, 33b, 181c, 568 and 576) are differentially expressed between resting and activated CD4+ T cells. In this study, we focused on the function of miR-568 during CD4+ T-cell activation. We showed that the expression level of miR-568 decreased during the activation of T cells, including Jurkat cells and human peripheral blood CD4+ T cells. When Jurkat or human peripheral blood CD4+ T cells were transfected with miR-568 mimics, cell activation was significantly inhibited, as shown by the inhibited expression of activation markers such as CD25, CD69 and CD154; decreased IL-2 production; and inhibited cell proliferation. Using software predictions and confirmatory experiments, we demonstrated that nuclear factor of activated T cells 5 (NFAT5) is a target of miR-568. Treg cells are an important CD4+ T-cell subpopulation, so we also evaluated the function of miR-568 in Treg-cell activation and differentiation. We showed that the miR-568 level decreased, while the NFAT5 protein level increased during CD4+CD25+ Treg-cell activation, and the transfection of miR-568 mimics inhibited the NFAT5 expression, inhibited the production of both TGF-β and IL-10 and also inhibited the proliferation of Treg cells. Our further study showed that over-expression of miR-568 can inhibit Treg-cell differentiation and can inhibit the suppressive effect of these cells on effector cells. In addition, inhibition of NFAT5 by siRNA-mediated knockdown can inhibit the activation and differentiation of Treg cells. These findings reveal that miR-568 can inhibit the activation and function of both CD4+ T cells and Treg cells by targeting NFAT5. Since miR-568 plays an important role in both CD4+ T cells and Treg cells, these findings may provide leads for the development of novel treatments for human inflammatory and autoimmune diseases.
- Published
- 2013
18. Identification of tubulin beta chain, thymosin beta-4-like protein 3, and cytochrome b-c₁ complex subunit 1 as serological diagnostic biomarkers of gastric cancer
- Author
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Nai-Jun, Fan, Ke, Li, Qing-Yin, Liu, Xiu-Li, Wang, Liang, Hu, Jun-Tang, Li, and Chun-Fang, Gao
- Subjects
Adenoma ,Male ,Gene Expression ,Middle Aged ,Sensitivity and Specificity ,Mass Spectrometry ,Thymosin ,Stomach Neoplasms ,Tubulin ,Case-Control Studies ,Biomarkers, Tumor ,Humans ,Protein Isoforms ,Female ,Carrier Proteins ,Aged - Abstract
Despite major advances in its diagnosis and treatment, gastric cancer (GC) remains a major life-threatening disease. Treatment of the disease is further aggravated by the lack of diagnostic biomarkers that can aid in the early detection of GC and promote its favorable prognosis. The present work aims to identify novel diagnostic biomarkers for GC.The present work is a case-control study that focuses on proteomic analysis of serum from healthy volunteers and GC patients using ClinProt profiling technology based on mass spectrometry. A pattern of proteins/peptides with the ability to differentiate the studied populations was identified. Deregulated proteins/peptides differentially expressed in the serum of patients compared with healthy volunteers were identified by mass spectroscopy.A pattern of proteins/peptides consisting of four protein/peptide peaks at m/z 1467, 1867, 2701, and 2094 was identified. These protein/peptide peaks were able to differentiate the studied populations with close to 100% sensitivity and specificity. Three of the deregulated proteins/peptides at m/z 1867, 2701, and 2094 were identified by mass spectroscopy (LTQ Orbitrap XL) as tubulin beta chain, thymosin beta-4-like protein 3, and cytochrome b-c₁ complex subunit 1, respectively.The pattern of proteins/peptides identified in the present work shows great potential for GC diagnosis. Deregulated proteins of tubulin beta chain, thymosin beta-4-like protein 3, and cytochrome b-c₁ complex subunit 1 may be involved in the pathogenesis of GC and serve as potential serological diagnostic biomarkers.
- Published
- 2013
19. Ectopically Expressed Perforin-1 Is Proapoptotic in Tumor Cell Lines by Increasing Caspase-3 Activity and the Nuclear Translocation of Cytochrome c
- Author
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Jing Zhao, Angang Yang, Libo Yao, Yun-Xin Cao, Yan-Ling Meng, Jun-Tang Li, Si-Yi Chen, Fang Wang, Lifeng Wang, Yan-Ming Xu, Wei-Hong Wen, and Lin-Tao Jia
- Subjects
Cell Physiology ,Anatomy and Physiology ,Immunology ,lcsh:Medicine ,Fluorescent Antibody Technique ,Apoptosis ,Phosphatidylserines ,Cell Line, Tumor ,Molecular Cell Biology ,Basic Cancer Research ,In Situ Nick-End Labeling ,Cytotoxic T cell ,Signaling in Cellular Processes ,Humans ,lcsh:Science ,Biology ,Apoptotic Signaling ,Oncogenic Signaling ,Multidisciplinary ,biology ,Cell Death ,Cell growth ,Caspase 3 ,Perforin ,lcsh:R ,Cell Cycle ,Degranulation ,Immunity ,Apoptosis Inducing Factor ,Cytochromes c ,Hep G2 Cells ,Cell cycle ,Signaling in Selected Disciplines ,digestive system diseases ,Cell biology ,Granzyme B ,Granzyme ,Oncology ,Cancer cell ,biology.protein ,Medicine ,lcsh:Q ,Cellular Types ,Research Article ,Signal Transduction ,HeLa Cells - Abstract
Perforin-1 (PRF), a cytotoxic lymphocyte pore-forming protein, plays an important role in the action of cytotoxic T cells and natural killer cells in that it causes the lysis of abnormal body cells and the elimination of virus-infected cells and tumors. Upon degranulation, PRF inserts itself into the target cell's plasma membrane, forming a pore. The subsequent translocation of pro-apoptotic granzymes (including granzyme B, A, M et al.) into the cytoplasm provides the proteases with access to numerous protein substrates that promote apoptosis after cleavage. These proteases are believed to be the main executioners of target cell apoptosis. Although the PRF and granzyme components are both critical to this process and in some way involved in inducing cell death in target cells, the inhibition of tumor growth could still be efficient in granzyme-deficient mice. It is unclear whether PRF alone can suppress tumors. In this study, we discovered that forced ectopic expression of PRF alone, in the absence of granzymes, could mediate cell death in cancer cells. Notably, transient expression of both full-length and truncated active-form PRF in human Hep G2, SK-BR-3, and HeLa cells was found to induce apparent cell growth inhibition and cell death, as evidenced by chromosome condensation and DNA fragmentation, increased caspase-3 activity, and the release of apoptosis inducing factor (AIF) and cytochrome c from the mitochondria. This PRF-induced cell death could be abrogated by pan-caspase inhibitor (Z-VAD) and mitochondria protector (TAT-BH4). The implication of these results is that ectopically expressed PRF has apoptosis-inducing abilities, and PRF alone is sufficient to induce apoptotic cell death in cells with ectopic expression. Taking this into consideration, our results suggest the possibility of using PRF as a pro-apoptotic gene for tumor therapeutics.
- Published
- 2012
20. Subanesthetic dose of isoflurane protects against zymosan-induced generalized inflammation and its associated acute lung injury in mice
- Author
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Yan Lu, Daorong Peng, Lei Shang, Jun-Tang Li, Keliang Xie, Jinglan Mu, Genlin Ji, Lize Xiong, and Lichao Hou
- Subjects
Male ,Minimum alveolar concentration ,Multiple Organ Failure ,Acute Lung Injury ,Lung injury ,Critical Care and Intensive Care Medicine ,Sepsis ,chemistry.chemical_compound ,Mice ,medicine ,Animals ,Amitrole ,Inflammation ,Inhalation ,Isoflurane ,business.industry ,Superoxide Dismutase ,Zymosan ,medicine.disease ,Catalase ,Oxidative Stress ,chemistry ,Anesthesia ,Anesthetic ,Emergency Medicine ,Multiple organ dysfunction syndrome ,business ,medicine.drug - Abstract
Multiple organ dysfunction syndrome (MODS) is one of the leading causes of death in the intensive care unit. Organ failure especially lung injury is highly associated with the mortality for MODS patients. Volatile anesthetic isoflurane (ISO) is one of the most widely used anesthetic agents, and ISO anesthesia has been reported to improve the survival rate and organ function in sepsis/MODS models. However, the application of anesthetic dose ISO in critically ill patients is limited. Compared with i.v. anesthetic pentobarbital treatment, we showed that twice inhalation of ISO at subanesthetic dose (0.7%, 0.5 minimum alveolar concentration) alleviated lung injury at 24 h after zymosan (ZY) injection and increased the 7-day survival rate from 10% to 45% in mice. We also showed that ISO exerted its protection by significantly improving the activities of superoxide dismutase and catalase in lung and serum when compared with those in pentobarbital-treated mice. The catalase inhibitor 3-amino-1, 2, 4-triazole partially abolished the protective effect of ISO in ZY-challenged mice. We conclude that subanesthetic dose ISO protects against ZY-induced generalized inflammation and its associated lung injury via enhancing the activities of antioxidant enzymes in mice, which may provide a new strategy for the treatment of critically ill patients.
- Published
- 2010
21. Support vector machine and genetic algorithm based predictive control for active power filter
- Author
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Shao-sheng Fan and Jun-tang Li
- Subjects
Support vector machine ,Engineering ,Model predictive control ,Adaptive control ,Automatic control ,Automatic Generation Control ,business.industry ,Control theory ,Internal model ,AC power ,business ,Active filter - Abstract
A new control method for active power filters using support vector machine (SVM) is presented. In the strategy, SVM is employed to model and predict future harmonic compensating current, it has the advantages of nonexistence of local minima solutions, automatic choice of model complexity and good generalization performance. Based on the model output, Genetic algorithm optimization method is adopted to produce proper value of control vector, this value is adequately modulated by means of a space vector PWM modulator which generate proper gating patterns of the inverter switches to maintain tracking of reference current. The SVM based predictive algorithm is used in internal model control scheme to compensate for process disturbances, measurement noise and modeling errors. The proposed method is applied to the control of a shunt active power filter, simulation results show SVM based predictive controller is more effective and feasible than PI control or digit adaptive control.
- Published
- 2008
22. Nuclear factor of activated T cells 5 maintained by Hotair suppression of miR-568 upregulates S100 calcium binding protein A4 to promote breast cancer metastasis.
- Author
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Jun-Tang Li, Li-Feng Wang, Ya-Li Zhao, Tao Yang, Wei Li, Jing Zhao, Feng Yu, Lei Wang, Yan-Ling Meng, Ning-Ning Liu, Xiao-Shan Zhu, Chun-Fang Gao, and Lin-Tao Jia
- Subjects
T cells ,IMMUNOSUPPRESSION ,CALCIUM ,BREAST cancer ,METASTASIS - Abstract
Introduction The onset of distal metastasis, which underlies the high mortality of breast cancers, warrants substantial studies to depict its molecular basis. Nuclear factor of activated T cells 5 (NFAT5) is up-regulated in various malignancies and is critically involved in migration and invasion of neoplastic cells. Nevertheless, the metastasis-related events potentiated by this transcriptional factor and the mechanism responsible for NFAT5 elevation in carcinoma cells remain to be fully elucidated. Methods The correlation of NFAT5 with breast cancer invasiveness was investigated in vitro and clinically. The genes transcriptionally activated by NFAT5 were probed and their roles in breast cancer progression were dissected. The upstream regulators of NFAT5 were studied with particular attempt to explore the involvement of non-coding RNAs, and the mechanism underlying the maintenance of NFAT5 expression was deciphered. Results In metastatic breast cancers, NFAT5 promotes epithelial-mesenchymal transition (EMT) and invasion of cells by switching on the expression of the calcium binding protein S100A4, and facilitates the angiogenesis of breast epithelial cells and thus the development of metastases by transcriptionally activating vascular endothelial growth factor C (VEGF-C). NFAT5 is directly targeted by miR-568, which is in turn suppressed by the long non-coding RNA, Hotair, via a documented in trans gene silencing pattern, that is recruitment of the polycomb complex (Polycomb Repressive Complex 2; PRC2) and LSD1, and consequently methylation of histone H3K27 and demethylation of H3K4 on the miR-568 loci. Conclusion This study unravels a detailed role of NFAT5 in mediating metastatic signaling, and provides broad insights into the involvement of Hotair, in particular, by transcriptionally regulating the expression of microRNA(s), in the metastasis of breast cancers. [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
23. Support vector machine and genetic algorithm based predictive control for active power filter.
- Author
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Jun-tang Li and Shao-sheng Fan
- Published
- 2008
- Full Text
- View/download PDF
24. Subanesthetic Isoflurane Reduces Zymosan-Induced Inflammation in Murine Kupffer Cells by Inhibiting ROS-Activated p38 MAPK/NF-κB Signaling.
- Author
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Hui Wang, Lei Wang, Nan-lin Li, Jun-tang Li, Feng Yu, Ya-li Zhao, Ling Wang, Jun Yi, Jie-fang Bian, Jiang-hao Chen, Shi-fang Yuan, Ting Wang, Yong-gang Lv, Ning-ning Liu, Xiao-shan Zhu, Rui Ling, and Jun Yun
- Published
- 2014
- Full Text
- View/download PDF
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