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| 1 | Upregulation of Chemokine CXCL12 in the Dorsal Root Ganglia and Spinal Cord Contributes to the Development and Maintenance of Neuropathic Pain Following Spared Nerve Injury in Rats显示文摘Emerging evidence indicates that CXCL12/CXCR4 signaling is involved in chronic pain. However, few studies have systemically assessed its role in direct nerve injury-induced neuropathic pain and the underlying mechanism. Here, we determined that spared nerve injury(SNI)increased the expression of CXCL12 and its cognate receptor CXCR4 in lumbar 5 dorsal root ganglia(DRG)neurons and satellite glial cells. SNI also induced longlasting upregulation of CXCL12 and CXCR4 in the ipsilateral L4–5 spinal cord dorsal horn, characterized by CXCL12 expression in neurons and microglia, and CXCR4 expression in neurons and astrocytes. Moreover, SNIinduced a sustained increase in TNF-a expression in the DRG and spinal cord. Intraperitoneal injection(i.p.) of the TNF-a synthesis inhibitor thalidomide reduced the SNI-induced mechanical hypersensitivity and inhibited the expression of CXCL12 in the DRG and spinal cord.Intrathecal injection(i.t.) of the CXCR4 antagonist AMD3100, both 30 min before and 7 days after SNI,reduced the behavioral signs of allodynia. Rats given an i.t.or i.p. bolus of AMD3100 on day 8 of SNI exhibited attenuated abnormal pain behaviors. The neuropathic pain established following SNI was also impaired by i.t. administration of a CXCL12-neutralizing antibody. Moreover,repetitive i.t. AMD3100 administration prevented the activation of ERK in the spinal cord. The mechanical hypersensitivity induced in na?¨ve rats by i.t. CXCL12 was alleviated by pretreatment with the MEK inhibitor PD98059. Collectively, our results revealed that TNF-a might mediate the upregulation of CXCL12 in the DRG and spinal cord following SNI, and that CXCL12/CXCR4 signaling via ERK activation contributes to the development and maintenance of neuropathic pain. | Liying Bai Xinru Wang Zhisong Li Cunlong Kong Yonghui Zhao Jun-Liang Qian Quancheng Kan Wei Zhang Ji-Tian Xu | 2016 | Neuroscience Bulletin2016，32，1： | 20 |
| 2 | Circulating tumor DNA 5-hydroxymethylcytosine as a novel diagnostic biomarker for esophageal cancer显示文摘 | Xin Tian Baofa Sun Chuanyuan Chen Chunchun Gao Ji Zhang XingYu Lu Linchen Wang Xiangnan Li Yurong Xing Ruijuan Liu Xiao Han Zheng Qi Xiaojian Zhang Chuan He Dali Han Yun-Gui Yang Quancheng Kan | 2018 | Cell Research2018，28，5： | 12 |
| 3 | Involvement of long non-coding RNAs in the progression of esophageal cancer显示文摘Esophageal cancer(EC)is one of the most common malignant tumors of the digestive system with high incidence and mortality rate worldwide.Therefore,exploring the pathogenesis of ECand searching for new targeted therapies are the current research hotspot for EC treatment.Long non-coding RNAs(lncRNAs)are endogenous RNAs with more than 200 nucleotides,but without proteincoding function.In recent years,lncRNAs have gradually become the focuses in the field of non-coding RNA.Some lncRNAs have been proved to be closely related to the pathogenesis of EC.Many lncRNAs are abnormally expressed in EC and participate in many biological processes including cell proliferation,apoptosis,and metastasis by inhibiting or promoting target gene expression.LncRNAs can also regulate the progression of EC through epithelial-mesenchymal transformation(EMT),which is closely related to the occurrence,development,and prognosis of EC.In this article,we review and discuss the involvement of lncRNAs in the progression of EC. | Wenhua Xue Yuanyuan Zheng Zhibo Shen Lifeng Li Zhirui Fan Wenbin Wang Zijia Zhu Yunkai Zhai Jie Zhao Quancheng Kan | 2021 | Cancer Communications2021，41，5： | 4 |
| 4 | Effect of oxymatrine on interferon-gamma and tumor necrosis factor-alpha serum levels in an experimental rat model of autoimmune encephalomyelitis显示文摘BACKGROUND:Studies have demonstrated that experimental autoimmune encephalomyelitis(EAE) onset correlates with increased interferon-γ(IFN-γ) and tumor necrosis factor-α(TNF-α) expression.Oxymatrine(OM) has been shown to inhibit autoimmune responses,but there are no reports showing that it could prevent the development of EAE.OBJECTIVE:To observe the effect of OM on serum levels of IFN-γ and TNF-α in a rat model of EAE.DESIGN,TIME AND SETTING:A randomized,controlled,animal study was performed at the Experimental Animal Center of Henan Academy of Chinese Medicine and at the Key Disciplines Laboratory Clinical Medicine of Henan Province between July and December 2008.MATERIALS:OM was purchased from Chia-tai Tianqing Pharmaceutical,China;complete Freund's adjuvant was purchased from Sigma,USA.METHODS:Forty female Wistar rats were randomly assigned to four groups:EAE model(M),low-dose OM treatment(OM-L),high-dose OM treatment(OM-H),and normal control(N,no immunization),with 10 rats in each group.EAE was established in the M,OM-L,and OM-H groups following immunization with Guinea pig spinal cord homogenate and complete Freund's adjuvant.The M and N groups were intraperitoneally injected with normal saline(6.7 mL/kg per day),the OM-L group received an intraperitoneal injection of OM(100 mg/kg per day),and the OM-H group received OM(150 mg/kg per day).MAIN OUTCOME MEASURES:At 16 days after immunization,the degree of histopathological changes in the spinal cord was assessed by hematoxylin-eosin stanining.Enzyme-linked immunosorbent assay was used to detect serum levels of IFN-γ,and radioimmunoassay was utilized to determine serum TNF-α level.Neurological scores were measured on a daily basis according to a 0-5 scale.RESULTS:Daily injections of OM,both high and low doses,resulted in decreased neurological scores in EAE rats(P < 0.01),as well as reduced cellular infiltration in the spinal cord and decreased levels of serum IFN-γ and TNF-α(P < 0.01).CONCLUSION:OM reduced the onset and severity of EAE,which correlated with decreased IFN-γ and TNF-α expression. | Xiaobin Guo Quancheng Kan Yifan Song Lin Zhu Xiang Li Haiying Hua GuangxianZhang | 2010 | Neural Regeneration Research2010，5，10： | 2 |
| 5 | Heparin inhibits burn-induced spleen cell apoptosis by suppressing interleukin-1 expression显示文摘 | Zhao Songfeng Zhang Xiao Zhang Xiaojian Shi Xiuqin Yu Zujiang Kan Quancheng | 2014 | Chinese Medical Journal2014，，13： | 1 |
| 6 | Ammonia-induced energy disorders interfere with bilirubin metabolism in hepatocytes显示文摘 | Qiongye Wang Yanfang Wang Zujiang Yu Duolu Li Bin Jia Jiangjing Li Kelei Guan Yubing Zhou Yanling Chen Quancheng Kan | 2014 | Archives of Biochemistry and Biophysics2014，，： | 1 |
| 7 | NSUN2-mediated mRNA m^(5)C Modification Regulates the Progression of Hepatocellular Carcinoma显示文摘RNA modifications affect many biological processes and physiological diseases.The 5-methylcytosine(m^(5)C)modification regulates the progression of multiple tumors.However,its characteristics and functions in hepatocellular carcinoma(HCC)remain largely unknown.Here,we found that HCC tissues had a higher m^(5)C methylation level than the adjacent normal tissues.Transcriptome analysis revealed that the hypermethylated genes mainly participated in the phosphokinase signaling pathways,such as the Ras and PI3K-Akt pathways.The m^(5)C methyltransferase NSUN2 was highly expressed in HCC tissues.Interestingly,the expression of many genes was positively correlated with the expression of NSUN2,including GRB2,RNF115,AATF,ADAM15,RTN3,and HDGF.Real-time PCR assays further revealed that the expression of the mRNAs of GRB2,RNF115,and AATF decreased significantly with the down-regulation of NSUN2 expression in HCC cells.Furthermore,NSUN2 could regulate the cellular sensitivity of HCC cells to sorafenib via modulating the Ras signaling pathway.Moreover,knocking down NSUN2 caused cell cycle arrest.Taken together,our study demonstrates the vital role of NSUN2 in the progression of HCC. | Dan Song Ke An Wenlong Zhai Luyao Feng Yingjie Xu Ran Sun Yueqin Wang Yun-Gui Yang Quancheng Kan Xin Tian | 2023 | Genomics, Proteomics & Bioinformatics2023，21，4： | 1 |
| 8 | RNA Structural Dynamics Modulate EGFR-TKI Resistance Through Controlling YRDC Translation in NSCLC Cells显示文摘Epidermal growth factor receptor-tyrosine kinase inhibitors(EGFR-TKIs)positively affect the initial control of non-small cell lung cancer(NSCLC).Rapidly acquired resistance to EGFR-TKIs is a major hurdle in successful treatment.However,the mechanisms that control the resistance of EGFR-TKIs remain largely unknown.RNA structures have widespread and crucial functions in many biological regulations;however,the functions of RNA structures in regulating cancer drug resistance remain unclear.Here,the psoralen analysis of RNA interactions and structures(PARIS)method is used to establish the higher-order RNA structure maps of EGFRTKIs-resistant and-sensitive cells of NSCLC.Our results show that RNA structural regions are enriched in untranslated regions(UTRs)and correlate with translation efficiency(TE).Moreover,yrdC N6-threonylcarbamoyltransferase domain containing(YRDC)promotes resistance to EGFR-TKIs.RNA structure formation in YRDC 30 UTR suppresses embryonic lethal abnormal vision-like 1(ELAVL1)binding,leading to EGFR-TKI sensitivity by impairing YRDC translation.A potential therapeutic strategy for cancer treatment is provided using antisense oligonucleotide(ASO)to perturb the interaction between RNA and protein.Our study reveals an unprecedented mechanism through which the RNA structure switch modulates EGFR-TKI resistance by controlling YRDC mRNA translation in an ELAVL1-dependent manner. | Boyang Shi Ke An Yueqin Wang Yuhan Fei Caixia Guo Qiangfeng Cliff Zhang Yun-Gui Yang Xin Tian Quancheng Kan | 2023 | Genomics, Proteomics & Bioinformatics2023，21，4： | 1 |
| 9 | CYP3A4 * 1G genetic polymorphism influences CYP3A activity and response to fentanyl in Chinese gynecologic patients显示文摘 | ZHANG Wei CHANG Yanzi KAN Quancheng | 2010 | Eur J Clin Pharmacol2010，66，1： | 1 |
| 10 | MiR-9 promotes the neural differentiation of mouse bone marrow mesenchymal stem cells via targeting zinc finger protein 521 显示文摘 | HAN Rui KAN Quancheng SUN Yingpu | 2012 | Neurosci Lett2012，515，2： | 1 |
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