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| 1 | Identification of RET gene fusion by exon array analyses in "pan-negative" lung cancer from never smokers显示文摘 | Li, Fei Feng, Yan Fang, Rong Fang, Zhaoyuan Xia, Jufeng Han, Xiangkun Liu, Xin-Yuan Chen, Haiquan Liu, Hongyan Ji, Hongbin | 2012 | Cell Research2012，22，5： | 11 |
| 2 | dentification of TRA2B-DNAH5 fusion as a novel oncogenic driver in human lung squamous cell carcinoma显示文摘 | Fei Li Zhaoyuan Fang Jian Zhang Chen Li Hongyan Liu Jufeng Xia Hongwen Zhu Chenchen auo Zhen Qin Fuming Li Xiangkun Han Yuetong Wang Yan Feng Ye Wang Wenjing Zhang Zuoyun Wang Yujuan Jin Yihua Sun Wenyi Wei Rong Zeng Haiquan Chen Hongbin Ji | 2016 | Cell Research2016，26，10： | 9 |
| 3 | QKI-5 regulates the alternative splicing of cytoskeletal gene ADD3 in lung cancer显示文摘Accumulating evidence indicates that the alternative splicing program undergoes extensive changes during cancer develop-ment and progression.The RNA-binding protein QKI-5 is frequently downregulated and exhibits anti-tumor activity in lung cancer.Howeve-r,little is known about the functional targets and regulatory mechanism of QKI-5.Here,we report that upregulation of exon 14 inclusion of cytoskeletal gene Adducin 3(ADD3)significantly correlates with a poor prognosis in lung cancer.QKI-5 inhibits cell proliferation and migration in part through suppressing the splicing of ADD3 exon 14.Through genome-wide mapping of QKI-5 binding sites in vivo at nucleotide resolution by iCLIP-seq analysis,we found that QKI-5 regulates alternative splicing of its target mRNAs in a binding position-dependent manner.By binding to multiple sites in an upstream intron region,QKI-5 represses the splicing of ADD3 exon 14.We also identified several QKI mutations in tumors,which cause dysregulation of the splicing of QKI targets ADD3 and NUMB.Taken together,our results reveal that QKI-mediated alternative splicing of ADD3 is a key lung cancer-associated splicing event,which underlies in part the tumor suppressor function of QKI. | Jin-Zhu Wang Xing Fu Zhaoyuan Fang Hui Liu Feng-Yang Zong Hong Zhu Yan-Fei Yu Xiao-Ying Zhang Shen-Fei Wang Ying Huang jingyi Hui | 2021 | Journal of Molecular Cell Biology2021，13，5： | 4 |
| 4 | Dynamic edge-based biomarker non-invasively predicts hepatocellular carcinoma with hepatitis B virus infection for individual patients based on blood testing显示文摘Hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC) is a major cause of cancer-related deaths in Asia and Africa. Developing effective and non-invasive biomarkers of HCC for individual patients remains an urgent task for early diagnosis and convenient monitoring. Analyzing the transcriptomic profiles of peripheral blood mononuclear cells from both healthy donors and patients with chronic HBV infection in different states (i.e. HBV carrier, chronic hepatitis B, cirrhosis, and HCC), we identified a set of 19 candidate genes according to our algorithm of dynamic network biomarkers. These genes can both characterize different stages during HCC progression and identify cirrhosis as the critical transition stage before carcinogenesis. The interaction effects (i.e. coexpressions) of candidate genes were used to build an accurate prediction model: the so-called edge-based biomarker. Considering the convenience and robustness of biomarkers in clinical applications, we performed functional analysis, validated candidate genes in other independent samples of our collected cohort, and finally selected COL5A1, HLA-DQB1, MMP2, and CDK4 to build edge panel as prediction models. We demonstrated that the edge panel had great performance in both diagnosis and prognosis in terms of precision and specificity for HCC, especially for patients with alpha-fetoprotein-negative HCC. Our study not only provides a novel edge-based biomarker for non-invasive and effective diagnosis of HBV-associated HCC to each individual patient but also introduces a new way to integrate the interaction terms of individual molecules for clinical diagnosis and prognosis from the network and dynamics perspectives. | Yiyu Lu Zhaoyuan Fang Meiyi Li Chen Qian Tao Zeng Lina Lu Qilong Chen Hui Zhang Qianmei Zhou Yan Sun Xuefeng Xue Yiyang Hu Luonan Chen Shibing Su | 2019 | Journal of Molecular Cell Biology2019，11，8： | 3 |
| 5 | A network-based gene-weighting approach for pathway analysis显示文摘古典算法瞄准与学习有关显著地识别生物小径调节经常减少的小径到基因集合,与对在一条定义小径以内的各种各样的基因的组成的非等价的明显的无知。我们这里设计了一个基于网络的方法以基因重量决定如此的非等价。决定的基因重量生物学上一致、柔韧联网不安。由把基因重量集成到古典基因设置分析,与为 “ 的随后的修正; over-counting”与多子单元蛋白质联系的偏爱,我们开发了一条新奇称基因的小径分析途径,在称为 “ 的一个 R 包裹实现了基因 Associaqtion 基于网络的小径 Analysis”(GANPA ) 。通过几 microarray 数据集的分析,包括 p53 数据集,气喘数据集和三乳癌数据集,我们证明我们的途径是生物学上可靠、可再现、对 microarray 因此有用的数据解释和假设产生。 | Zhaoyuan Fang Weidong Tian Hongbin Ji | 2012 | Cell Research2012，22，3： | 2 |
| 6 | c-CSN:Single-cell RNA Sequencing Data Analysis by Conditional Cell-specific Network显示文摘t The rapid advancement of single-cell technologies has shed new light on the complex mechanisms of cellular heterogeneity.However,compared to bulk RNA sequencing(RNA-seq),single-cell RNA-seq(scRNA-seq)suffers from higher noise and lower coverage,which brings new computational difficulties.Based on statistical independence,cell-specific network(CSN)is able to quantify the overall associations between genes for each cell,yet suffering from a problem of overestimation related to indirect effects.To overcome this problem,we propose the c-CSN method,which can construct the conditional cell-specific network(CCSN)for each cell.c-CSN method can measure the direct associations between genes by eliminating the indirect associations.c-CSN can be used for cell clustering and dimension reduction on a network basis of single cells.Intuitively,each CCSN can be viewed as the transformation from less“reliable”gene expression to more“reliable”gene–gene associations in a cell.Based on CCSN,we further design network flow entropy(NFE)to estimate the differentiation potency of a single cell.A number of scRNA-seq datasets were used to demonstrate the advantages of our approach.1)One direct association network is generated for one cell.2)Most existing scRNA-seq methods designed for gene expression matrices are also applicable to c-CSN-transformed degree matrices.3)CCSN-based NFE helps resolving the direction of differentiation trajectories by quantifying the potency of each cell.c-CSN is publicly available at https://github.com/LinLi-0909/c-CSN. | Lin Li Hao Dai Zhaoyuan Fang Luonan Chen | 2021 | Genomics, Proteomics & Bioinformatics2021，19，2： | 2 |
| 7 | Counteracting lineage-specific transcription factor network finely tunes lung adeno-to-squamous transdifferentiation through remodeling tumor immune microenvironment显示文摘Human lung adenosquamous cell carcinoma(LUAS),containing both adenomatous and squamous pathologies,harbors strong plasticity and is significantly associated with poor prognosis.We established an up-to-date comprehensive genomic and transcriptomic landscape of LUAS in 109 Chinese specimens and demonstrated LUAS development via adeno-to-squamous transdifferentiation.Unsupervised transcriptomic clustering and dynamic network biomarker analysis identified an inflammatory subtype as the critical transition stage during LUAS development.Dynamic dysregulation of the counteracting lineage-specific transcription factors(TFs),containing adenomatous TFs NKX2-1 and FOXA2,and squamous TFs TP63 and SOX2,finely tuned the lineage transition via promoting CXCL3/5-mediated neutrophil infiltration.Genomic clustering identified the most malignant subtype featured with STK11-inactivation,and targeting LSD1 through genetic deletion or pharmacological inhibition almost eradicated STK11-deficient lung tumors.These data collectively uncover the comprehensive molecular landscape,oncogenic driver spectrum and therapeutic vulnerability of Chinese LUAS. | Shijie Tang Yun Xue Zhen Qin Zhaoyuan Fang Yihua Sun Chongzhe Yuan Yunjian Pan Yue Zhao Xinyuan Tong Jian Zhang Hsinyi Huang Yuting Chen Liang Hu Dasong Huang Ruiqi Wang Weiguo Zou Yuan Li Roman KThomas Andrea Ventura Kwok-Kin Wong Haiquan Chen Luonan Chen Hongbin Ji | 2023 | National Science Review2023，10，4： | 0 |
| 8 | Oxidative stress-triggered Wnt signaling perturbation characterizes the tipping point of lung adeno-to-squamous transdifferentiation显示文摘Lkb1 deficiency confers the Kras-mutant lung cancer with strong plasticity and the potential for adeno-to-squamous transdifferentiation(AST).However,it remains largely unknown how Lkb1 deficiency dynamically regulates AST.Using the classical AST mouse model(Kras LSL-G12D/+;Lkb1flox/flox,KL),we here comprehensively analyze the temporal transcriptomic dynamics of lung tumors at different stages by dynamic network biomarker(DNB)and identify the tipping point at which the Wnt signaling is abruptly suppressed by the excessive accumulation of reactive oxygen species(ROS)through its downstream effector FOXO3A.Bidirectional genetic perturbation of the Wnt pathway using two different Ctnnb1 conditional knockout mouse strains confirms its essential role in the negative regulation of AST.Importantly,pharmacological activation of the Wnt pathway before but not after the tipping point inhibits squamous transdifferentiation,highlighting the irreversibility of AST after crossing the tipping point.Through comparative transcriptomic analyses of mouse and human tumors,we find that the lineage-specific transcription factors(TFs)of adenocarcinoma and squamous cell carcinoma form a“Yin-Yang”counteracting network.Interestingly,inactivation of the Wnt pathway preferentially suppresses the adenomatous lineage TF network and thus disrupts the“Yin-Yang”homeostasis to lean towards the squamous lineage,whereas ectopic expression of NKX2-1,an adenomatous lineage TF,significantly dampens such phenotypic transition accelerated by the Wnt pathway inactivation.The negative correlation between the Wnt pathway and AST is further observed in a large cohort of human lung adenosquamous carcinoma.Collectively,our study identifies the tipping point of AST and highlights an essential role of the ROS-Wnt axis in dynamically orchestrating the homeostasis between adeno-and squamous-specific TF networks at the AST tipping point. | Zhaoyuan Fang Xiangkun Han Yueqing Chen Xinyuan Tong Yun Xue Shun Yao Shijie Tang Yunjian Pan Yihua Sun Xue Wang Yujuan Jin Haiquan Chen Liang Hu Lijian Hui Lin Li Luonan Chen Hongbin Ji | 2023 | Signal Transduction and Targeted Therapy2023，8，2： | 0 |
| 9 | Single-Atomic Site Catalyst Enhanced Lateral Flow Immunoassay for Point-of-Care Detection of Herbicide显示文摘Point-of-care(POC)detection of herbicides is of great importance due to their impact on the environment and potential risks to human health.Here,we design a single-atomic site catalyst(SASC)with excellent peroxidase-like(POD-like)catalytic activity,which enhances the detection performance of corresponding lateral flow immunoassay(LFIA).The iron single-atomic site catalyst(Fe-SASC)is synthesized from hemin-doped ZIF-8,creating active sites that mimic the Fe active center coordination environment of natural enzyme and their functions.Due to its atomically dispersed iron active sites that result in maximum utilization of active metal atoms,the Fe-SASC exhibits superior POD-like activity,which has great potential to replace its natural counterparts.Also,the catalytic mechanism of Fe-SASC is systematically investigated.Utilizing its outstanding catalytic activity,the Fe-SASC is used as label to construct LFIA(Fe-SASC-LFIA)for herbicide detection.The 2,4-dichlorophenoxyacetic acid(2,4-D)is selected as a target here,since it is a commonly used herbicide as well as a biomarker for herbicide exposure evaluation.A linear detection range of 1-250 ng/mL with a low limit of detection(LOD)of 0.82 ng/mL has been achieved.Meanwhile,excellent specificity and selectivity towards 2,4-D have been obtained.The outstanding detection performance of the Fe-SASC-LFIA has also been demonstrated in the detection of human urine samples,indicating the practicability of this POC detection platform for analyzing the 2,4-D exposure level of a person.We believe this proposed Fe-SASC-LFIA has potential as a portable,rapid,and high-sensitive POC detection strategy for pesticide exposure evaluation. | Zhaoyuan Lyu Shichao Ding Peter Tieu Lingzhe Fang Xin Li Tao Li Xiaoqing Pan Mark H.Engelhard Xiaofan Ruan Dan Du Suiqiong Li Yuehe Lin | 2023 | Research2023，，1： | 0 |
| 10 | Targeting HSPA1A in ARID2-deficient lung adenocarcinoma显示文摘Somatic mutations of the chromatin remodeling gene ARID2 are observed in~7%of human lung adenocarcinomas(LUADs).However,the role of ARID2 in the pathogenesis of LUADs remains largely unknown.Here we find that ARID2 expression is decreased during the malignant progression of both human and mice LUADs.Using two Kras^(G12D)-based genetically engineered murine models,we demonstrate that ARID2 knockout significantly promotes lung cancer malignant progression and shortens overall survival.Consistently,ARID2 knockdown significantly promotes cell proliferation in human and mice lung cancer cells.Through integrative analyses of Ch IP-Seq and RNA-Seq data,we find that Hspa1 a is up-regulated by Arid2 loss.Knockdown of Hspa1 a specifically inhibits malignant progression of Arid2-deficient but not Arid2-wt lung cancers in both cell lines as well as animal models.Treatment with an HSPA1 A inhibitor could significantly inhibit the malignant progression of lung cancer with ARID2 deficiency.Together,our findings establish ARID2 as an important tumor suppressor in LUADs with novel mechanistic insights,and further identify HSPA1 A as a potential therapeutic target in ARID2-deficient LUADs. | Xue Wang Yuetong Wang Zhaoyuan Fang Hua Wang Jian Zhang Longfu Zhang Hsinyi Huang Zhonglin Jiang Yujuan Jin Xiangkun Han Shenda Hou Bin Zhou Feilong Meng Luonan Chen Kwok-Kin Wong Jinfeng Liu Zhiqi Zhang Xin Zhang Haiquan Chen Yihua Sun Liang Hu Hongbin Ji | 2021 | National Science Review2021，8，10： | 0 |
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