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| 1 | E)NA sensor cGAS-mediated immune recognition显示文摘 | Pengyan Xia Shuo Wang Pu Gao Guangxia Gao Zusen Fan | 2016 | Protein & Cell2016，7，11： | 11 |
| 2 | Transdifferentiation of tumor infiltrating innate lymphoid cells during progression of colorectal cancer显示文摘Innate lymphoid cells(ILCs)reside in mucosal surfaces to potentiate immune responses,sustain mucosal integrity and maintain tissue homeostasis.However,how tumor infiltrating ILCs modulate tumor development and progression is unclear.Here we profiled tumor infiltrating ILCs during colorectal cancer(CRC)progression by single-cell RNA sequencing.We identified six clusters of tumor infiltrating ILCs with unique features.ILC1s expressed inhibitory receptors and underwent inhibitory functional conversion at the late stage of CRC.ILC2s were classified into three subsets(called ILC2-A,-B,-C),of which ILC2-C subset could facilitate tumor progression.HS3ST1 and PD1 were highly expressed in ILC2s of late stage CRC tumors and deficiency of HS3ST1 or PD1 in ILC2s suppressed tumor growth.Moreover,ILC3s transdifferentiated into ILCregs during CRC progression and ILCregs promoted tumor growth.Of note,TGF-βsignaling initiated the conversion of ILC3s to ILCregs and blockade of TGF-βsignaling could disrupt the ILCreg transdifferentiation and inhibited tumor growth.Thus,intervention of ILC conversions might be a potential strategy for CRC immunotherapy. | Shuo Wang Yuan Qu Pengyan Xia Yi Chen Xiaoxiao Zhu Jing Zhang Guan Wang Yong Tian Jianming Ying Zusen Fan | 2020 | Cell Research2020，30，7： | 9 |
| 3 | Gut microbiota drives macrophage-dependent self-renewal of intestinal stem cells via niche enteric serotonergic neurons显示文摘Lgr5+intestinal stem cells(ISCs)reside within specialized niches at the crypt base and harbor self-renewal and differentiation capacities.ISCs in the crypt base are sustained by their surrounding niche for precise modulation of self-renewal and differentiation.However,how intestinal cells in the crypt niche and microbiota in enteric cavity coordinately regulate ISC stemness remains unclear.Here,we show that ISCs are regulated by microbiota and niche enteric serotonergic neurons.The gut microbiota metabolite valeric acid promotes Tph2 expression in enteric serotonergic neurons via blocking the recruitment of the NuRD complex onto Tph2 promoter.5-hydroxytryptamine(5-HT)in turn activates PGE2 production in a PGE2+macrophage subset through its receptors HTR2A/3 A;and PGE2 via binding its receptors EP1/EP4,promotes Wnt/β-catenin signaling in ISCs to promote their self-renewal.Our findings illustrate a complex crosstalk among microbiota,intestinal nerve cells,intestinal immune cells and ISCs,revealing a new layer of ISC regulation by niche cells and microbiota. | Pingping Zhu Tiankun Lu Jiayi Wu Dongdong Fan Benyu Liu Xiaoxiao Zhu Hui Guo Ying Du Feng Liu Yong Tian Zusen Fan | 2022 | Cell Research2022，32，6： | 8 |
| 4 | Mutation profile and its correlation with clinicopathology in Chinese hepatocellular carcinoma patients显示文摘Background:Hepatocellular carcinoma(HCC)is one of the most common causes of cancer worldwide.Although many studies have focused on oncogene characteristics,the genomic landscape of Chinese HCC patients has not been fully clarified.Methods:A total of 165 HCC patients,including 146 males and 19 females,were enrolled.The median age was 55 years(range,27-78 years).Corresponding clinical and pathological information was collected for further analysis.A total of 168 tumor tissues from these patients were selected for next-generation sequencing(NGS)-based 450 panel gene sequencing.Genomic alterations including single nucleotide variations(SNV),short and long insertions and deletions(InDels),copy number variations,and gene rearrangements were analyzed.Tumor mutational burden(TMB)was measured by an algorithm developed in-house.The top quartile of HCC was classified as TMB high.Results:A total of 1,004 genomic alterations were detected from 258 genes in 168 HCC tissues.TMB values were identified in 160 HCC specimens,with a median TMB of 5.4 Muts/Mb(range,0-28.4 Muts/Mb)and a 75%TMB of 7.7 Muts/Mb.The most commonly mutated genes were TP53,TERT,CTNNB1,AXIN1,RB1,TSC2,CCND1,ARID1A,and FGF19.SNV was the most common mutation type and C:G>T:A and guanine transformation were the most common SNVs.Compared to wild-type patients,the proportion of Edmondson grade III-IV and microvascular invasion was significantly higher in TP53 mutated patients(P<0.05).The proportion of tumors invading the hepatic capsule was significantly higher in TERT mutated patients(P<0.05).The proportion of Edmondson grade I-II,alpha fetoprotein(AFP)<25μmg/L,and those without a history of hepatitis B was significantly higher in CTNNB1 mutated patients(P<0.05).CTNNB1 mutations were associated with TMB high in HCC patients(P<0.05).Based on correlation analysis,the mutation of TP53 was independently correlated with microvascular invasion(P=0.002,OR=3.096)and Edmondson grade III-IV(P=0.008,OR=2.613).The mutation of TERT was independently correlated with tumor invasion of the liver capsule(P=0.001,OR=3.030),and the mutation of CTNNB1 was independently correlated with AFP(<25μmg/L)(P=0.009,OR=3.414).Conclusions:The most frequently mutated genes of HCC patients in China were TP53,TERT,and CTNNB1,which mainly lead to the occurrence and development of HCC by regulating the P53 pathway,Wnt pathway,and telomere repair pathway.There were more patients with microvascular invasion and Edmondson III-IV grade in TP53 mutated patients and more patients with hepatic capsule invasion in TERT mutated patients,while in CTNNB1 mutated patients,there were more patients with Edmondson I-II grade,AFP<25μmg/L,and a non-hepatitis B background.Also,the TMB values were significantly higher in CTNNB1 mutated patients than in wild type patients. | Shuo Wang Huasheng Shi Tao Liu Manjiang Li Sanshun Zhou Xuan Qiu Zusen Wang Weiyu Hu Weidong Guo Xiaoqian Chen Honglin Guo Xiaoliang Shi Junping Shi Yunjin Zang Jingyu Cao Liqun Wu | 2021 | Hepatobiliary Surgery and Nutrition2021，10，2： | 8 |
| 5 | Cancer stem cells and tumorigenesis显示文摘 | Pingping Zhu Zusen Fan | 2018 | Biophysics Reports2018，4，4： | 7 |
| 6 | RNF2 is recruited by WASH to ubiquitinate AMBRA1 leading to downregulation of autophagy显示文摘洗(Wiskott-Aldrich 症候群蛋白质(黄蜂) 和疤相当或相同的事物) 被识别在经由 Arp2/3 激活排序的 endosomal 工作。我们以前表明了那洗在有 AMBRA1 的 BECN1-PIK3C3 建筑群是 BECN1 和现在的新 interactor。AMBRA1-DDB1-CUL4A 建筑群是为 BECN1 的连接 K63 的 ubiquitination 的 E3 ligase,它为导致饥饿的 autophagy 被要求。洗由 BECN1 ubiquitination 的抑制压制 autophagy。然而, AMBRA1 怎么在 autophagy 期间被调整,留下逃犯。这里,我们发现 RNF2 与 AMBRA1 联系经由 K48 连接充当 E3 ligase 到 ubiquitinate AMBRA1。RNF2 调停在离氨酸 45 点的 AMBRA1 的 ubiquitination。尤其是, RNF2 缺乏提高 autophagy 正式就职。在 autophagy 正式就职之上, RNF2 加强 AMBRA1 降级在的帮助下洗。洗缺乏与 AMBRA1 损害 RNF2 的协会阻碍 AMBRA1 降级。我们的调查结果揭示 autophagy 的规定的另一新奇的层通过为导致 autophagy 的 downregulation 的 AMBRA1 降级洗 RNF2 的招募。 | Pengyan Xia Shuo Wang Guanling Huang Ying Du Pingping Zhu Man Li Zusen Fan | 2014 | Cell Research2014，24，8： | 7 |
| 7 | Structural insights into the regulatory mechanism of the Pseudomonas aeruginosa YfiBNR system显示文摘 | Min Xu Xuan Yang Xiu-An Yang Lei Zhou Tie-Zheng Liu Zusen Fan Tao Jiang | 2016 | Protein & Cell2016，7，6： | 2 |
| 8 | Circular RNA circZbtb20 maintains ILC3 homeostasis and function via Alkbh5-dependent m6A demethylation of Nr4a1 mRNA显示文摘Group 3 innate lymphoid cells(ILC3s)play critical roles in innate immunity and gut homeostasis.However,how ILC3 homeostasis is regulated remains elusive.Here,we identified a novel circular RNA,circZbtb20,that is highly expressed in ILC3s and required for their maintenance and function.CircZbtb20 deletion causes reduced ILC3 numbers,increasing susceptibility to C.rodentium infection.Mechanistically,circZbtb20 enhances the interaction of Alkbh5 with Nr4a1 mRNA,leading to ablation of the m6A modification of Nr4a1 mRNA to promote its stability.Nr4a1 initiates Notch2 signaling activation,which contributes to the maintenance of ILC3 homeostasis.Deletion of Alkbh5 or Nr4a1 also impairs ILC3 homeostasis and increases susceptibilities to bacterial infection.Thus,our findings reveal an important role of circular RNA in the regulation of innate lymphoid cell homeostasis. | Benyu Liu Nian Liu Xiaoxiao Zhu Liuliu Yang Buqing Ye Huimu Li Pingping Zhu Tiankun Lu Yong Tian Zusen Fan | 2021 | Cellular & Molecular Immunology2021，18，6： | 2 |
| 9 | Tumor suppressor nm23 -H1 is a granzyme A -activated DNase during CTL-mediated apoptosis,and the nucleosome assembly protein SET is its inhibitor显示文摘 | Zusen Fan Paul J Bersford | 2003 | Cell2003，112，5： | 1 |
| 10 | Transient Activation of Autophagy via Sox2-Mediated Suppression of mTOR Is an Important Early Step in Reprogramming to Pluripotency显示文摘 | Shuo Wang Pengyan Xia Buqing Ye Guanling Huang Jing Liu Zusen Fan | 2013 | Cell Stem Cell2013，，5： | 1 |
| 11 | Tumor Suppressor NM23-H1 Is a Granzyme A-Activated DNase during CTL-Mediated Apoptosis, and the Nucleosome Assembly Protein SET Is Its Inhibitor显示文摘 | Zusen Fan Paul J. Beresford David Y. Oh Dong Zhang Judy Lieberman | 2003 | Cell2003，，5： | 1 |
| 12 | Tumor suppressor nm23-H1 is a granzyme A-activated DNase during CTL-mediated apoptosis,and the nucleosome assembly protein SET is its inhibitor显示文摘 | Zusen Fan Paul J Bersford | 2003 | Cell2003，112，5： | 1 |
| 13 | Molecular Mechanisms of Lymphocyte-Mediated Cytotoxicity显示文摘Granule-mediated cytotoxicity is the major mechanism for lymphocytes to kill viruses, intracellular bacteria and tumors. The cytotoxic granules move to the immunological synapse by exocytosis after recognition of a killer cell.The contents of the granules are delivered into target cells with the help of perforin by endocytosis. A group of serine protease granzymes cleave their critical substrates to initiate DNA damage and cell death. The most abundant granzymes are granzyme A and B. They induce cell death through alternate and nonoverlapping pathways. The substrates and functions of the majority of the orphan granzymes have not yet been identified. It is possible that the diversity of granzymes provides fail-safe mechanisms for killing viruses and tumor cells. | Zusen Fan Qixiang Zhang | 2005 | Cellular & Molecular Immunology2005，2，4： | 1 |
| 14 | Neurotrophin 3 hinders the growth and metastasis of hepatocellular carcinoma cells显示文摘Objective Neurotrophin 3(NTF3)is involved in numerous biological processes;however,its role in hepatocellular carcinoma(HCC)is not well studied.This study investigated NTF3 function in HCC progression and revealed its underlying molecular mechanisms.Methods The prognostic relevance of NTF3 was determined through a bioinformatical analysis of publicly available TCGA data.Immunohistochemistry of HCC biopsies was performed to explore the expression of NTF3.Cell growth and proliferation were analyzed using a Cell Counting Kit-8(CCK-8)assay.Cell invasion and migration were analyzed using Boyden Transwell and wound healing assays.Protein expression and mRNA levels were evaluated through immunoblotting and quantitative polymerase chain reaction(qPCR).Cell apoptosis was evaluated with flow cytometry.Results NTF3 expression was significantly lower in HCC tissues than in adjacent non-tumor tissues.Low NTF3 expression was significantly associated with decreased patient survival and specific clinicopathological features.NTF3 overexpression reduced the proliferation,migration,and invasion abilities of HCC cell lines.Conclusion Decreased expression of NTF3 is associated with poor prognosis in HCC patients,likely due to its action in promoting HCC cell proliferation,migration,and invasion.Our findings provide a novel understanding into the pathogenesis of HCC and the role of NTF3 in tumor progression,suggesting that targeting NTF3 has potential therapeutic and diagnostic value for HCC. | Shengnan Zhao Aixia Chen Jingyu Cao Zusen Wang Weiyu Hu Fei Zhou Donghai Liang Hongsheng Yu | 2020 | Oncology and Translational Medicine2020，6，4： | 0 |
| 15 | Regulation of noncoding RNAs in innate lymphoid cells显示文摘Innate lymphoid cells(ILCs)have been defined in recent years and are important effector cells against pathogens and critical regulators in maintaining tissue homeostasis[1].Noncoding RNAs(ncRNAs),such as circular RNAs(circRNAs),long noncoding RNAs(lncRNAs),and microRNAs(miRNAs),in ILCs are emerging and have been described to function in ILC biology.These ncRNAs are distributed with unique patterns in ILCs and function in different molecular mechanisms.Accumulating research evidence demonstrates that ncRNA dysregulation links ILC-mediated immune responses and diseases. | Benyu Liu Lingwei Zhang Pingping Zhu Zusen Fan | 2023 | Cellular & Molecular Immunology2023，20，5： | 0 |
| 16 | Noncoding RNAs in tumorigenesis and tumor therapy显示文摘Tumorigenesis is a complicated process in which numerous modulators are involved in different ways.Previous studies have focused primarily on tumor-associated protein-coding genes such as oncogenes and tumor suppressor genes,as well as their associated oncogenic pathways.However,noncoding RNAs(ncRNAs),rising stars in diverse physiological and pathological processes,have recently emerged as additional modulators in tumorigenesis.In this review,we focus on two typical kinds of ncRNAs:long noncoding RNAs(lncRNAs)and circular RNAs(circRNAs).We describe the molecular patterns of ncRNAs and focus on the roles of ncRNAs in cancer stem cells(CSCs),tumor cells,and tumor environmental cells.CSCs are a small subset of tumor cells and are generally considered to be cells that initiate tumorigenesis,and dozens of ncRNAs have been defined as critical modulators in CSC maintenance and oncogenesis.Moreover,ncRNAs are widely involved in oncogenetic processes,including sustaining proliferation,resisting cell death,genome instability,metabolic disorders,immune escape and metastasis.We also discuss the potential applications of ncRNAs in tumor diagnosis and therapy.The progress in ncRNA research greatly improves our understanding of ncRNAs in oncogenesis and provides new potential targets for future tumor therapy. | Pingping Zhu Benyu Liu Zusen Fan | 2023 | Fundamental Research2023，3，5： | 0 |
| 17 | Induction of functional neutrophils from mouse fibroblasts by thymidine through enhancement of Tet3 activity显示文摘Neutrophils are derived from bone marrow hematopoietic stem cells(HSCs)and are the largest population among circulating white blood cells in humans,acting as the first line of defense against invading pathogens.Whether neutrophils can be generated by transdifferentiation strategies is unknown.Here,we show that thymidine induces the conversion of mouse fibroblasts to neutrophils.Induced neutrophils(iNeus)showed antibacterial effects and did not undergo malignant transformation in vivo.Importantly,iNeu transplantation cured neutropenia in mice in vivo.Mechanistically,thymidine mediates iNeu conversion by enhancing Tet3 activity.Tet3 initiates the expression of the neutrophil fate decision factors Cebpδ and Rfx1 that drive the transdifferentiation of mouse fibroblasts to neutrophils.Therefore,the induction of functional neutrophils by chemicals may provide a potential therapeutic strategy for patients with neutropenia patients and infectious diseases. | Buqing Ye Liuliu Yang Benyu Liu Nian Liu Dongdong Fan Huimu Li Lei Sun Ying Du Shuo Wang Yong Tian Zusen Fan | 2022 | Cellular & Molecular Immunology2022，19，5： | 0 |
| 18 | Recombinant adenovirus vector-mediated human MDA-7 gene transfection suppresses hepatocellular carcinoma growth in a mouse xenograft model显示文摘Hepatocellular carcinoma is one of the most common tumors in the world.The purpose of the present study was to investigate the inhibitory effects of adenoviral transduction of human melanoma differentiation-associated gene-7(MDA-7)gene on hepatocellular carcinoma,so as to provide a theoretical basis for gene therapy of the disease.The human MDA-7 gene was cloned into replication-defective adenovirus specific to HepG2 cells using recombinant virus technology.RT-PCR and Western blotting assays were used to determine the expression of human MDA-7 mRNA and MDA-7 protein in HepG2 cells in vitro.Induction of apoptosis by overexpression of the human MDA-7 gene was determined by flow cytometry.In-vivo efficacy of adenoviral delivery of the human MDA-7 gene was assessed in nude mice bearing HepG2 cell lines in vivo by determining inhibition of tumor growth,VEGF and CD34 expression,and microvascular density(MVD).The results showed that AdGFP/MDA-7 induced apoptosis of HepG2 cells in vitro and significantly inhibited tumor growth in vivo(P < 0.05).The intra-tumoral MVD decreased significantly in the treated tumors(P < 0.05).We conclude the recombination adenovirus AdGFP/MDA-7 can effectively express biologically active human MDA-7,which leads to inhibition of hepatocellular carcinoma growth. | Xinting Pan Liqun Wu Jingyu Cao Weidong Guo Zusen Wang Bing Han Weiyu Hu | 2012 | The Journal of Biomedical Research2012，26，1： | 0 |
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