Yu Feng

Leman University

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Runsen Chen

Second Affiliated Hospital of Nanjing Medical University

Xuming Mo

Second Affiliated Hospital of Nanjing Medical University

Di Yu

Second Affiliated Hospital of Nanjing Medical University

Yang Zhang

Harbin Medical University

Tong Liu

Nantong University

Zhuo-Xian Meng

Shanxi Agricultural University

Shuo Li

Taizhou University

Ziniu Yu

Huazhong Agricultural University

Jian Xiong

Nanchang University

Ling Zhang

Nanchang University

Cooperative Institutions

Soochow University

147

Chinese Academy of Medical Sciences & Peking Union Medical College

101

Chinese Academy of Sciences

Shanghai Jiao Tong University

Nanjing Medical University

Sichuan University

Sun Yat-sen University

Zhejiang University

Second Affiliated Hospital of Soochow University

Peking University

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Identification of 67 pleiotropic genes for seven autoimmune diseases using multivariate statistical analysis

bioRxiv (Cold Spring Harbor Laboratory) (2019)

Xiaocan Jia Nian Shi Zhenhua Xia Yu Feng Yifan Li

Abstract Although genome-wide association studies (GWAS) have a dramatic impact on susceptibility locus discovery, this univariate approach has limitation in detecting complex genotype-phenotype correlations. It is essential to identify shared genetic risk factors acting through common biological mechanisms of autoimmune diseases with a multivariate analysis. In this study, the GWAS summary statistics including 41,274 single nucleotide polymorphisms (SNPs) located in 11,516 gene regions was analyzed to identify shared variants of seven autoimmune diseases using metaCCA method. Gene-based association analysis was used to refine the pleiotropic genes. In addition, GO term enrichment analysis and protein-protein interaction network analysis were applied to explore the potential biological function of the identified genes. After metaCCA analysis, 4,962 SNPs ( P <1.21×10 −6 ) and 1,044 pleotropic genes ( P <4.34×10 −6 ) were identified. By screening the results of gene-based p-values, we identified the existence of 27 confirmed pleiotropic genes and highlighted 40 novel pleiotropic genes which achieved significance threshold in metaCCA analysis and were also associated with at least one autoimmune disease in the VEGAS2 analysis. The metaCCA method could identify novel variants associated with complex diseases incorporating different GWAS datasets. Our analysis may provide insights for some common therapeutic approaches of autoimmune diseases based on the pleiotropic genes and common mechanisms identified. Author summary Although previous researches have clearly indicated varying degrees of overlapping genetic sensitivities in autoimmune diseases, it has proven GWAS only explain small percent of heritability. Here, we take advantage of recent technical and methodological advances to identify pleiotropic genes that act on common biological mechanisms and the overlapping pathophysiological pathways of autoimmune diseases. After selection using multivariate analysis and verification using gene-based analyses, we successfully identified a total of 67 pleiotropic genes and performed the functional term enrichment analysis. In particularly, 27 genes were identified to be pleiotropic in previous different types of studies, which were validated by our present study. Forty significant genes (16 genes were associated with one disease earlier, and 24 were novel) might be the novel pleiotropic candidate genes for seven autoimmune diseases. The improved detection not only yielded the shared genetic components but also provided better understanding for exploring the potential common biological pathogenesis of these major autoimmune diseases.

Genome-wide Association Study

Genetic Association

Candidate gene

10.1101/563973

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Citations (1)

Mechanisms of drugs-resistance in small cell lung cancer: DNA-related, RNA-related, apoptosis-related, drug accumulation and metabolism procedure

Translational Lung Cancer Research (2020)

Peixin Chen Peng Kuang Lei Wang Wei Li Bin Chen

Abstract: Small-cell lung cancer (SCLC), the highest malignant cancer amongst different types of lung cancer, has the feature of lower differentiation, rapid growth, and poor survival rate. Despite the dramatically initial sensitivity of SCLC to various types of treatment methods, including chemotherapy, radiotherapy and immunotherapy, the emergence of drugs-resistance is still a grandly clinical challenge. Therefore, in order to improve the prognosis and develop new therapeutic approaches, having a better understanding of the complex mechanisms of resistance in SCLC is of great clinical significance. This review summarized recent advances in understanding of multiple mechanisms which are involved in the resistance during SCLC treatment, including DNA-related process, RNA-related process, apoptosis-related mechanism, and the process of drug accumulation and metabolism.

10.21037/tlcr-19-547

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Citations (27)

TMEM105 modulates disulfidptosis and tumor growth in pancreatic cancer via the β-catenin-c-MYC-GLUT1 axis

International Journal of Biological Sciences (2025)

Yifan Yin Yixuan Sun Hong-Fei Yao Yu Feng Qin-Yuan Jia

10.7150/ijbs.104598

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Four-octyl itaconate activates Keap1-Nrf2 signaling to protect neuronal cells from hydrogen peroxide

Cell Communication and Signaling (2018)

Hua Liu Yu Feng Min Xu Jian Yang Zhichun Wang

Four-octyl itaconate (OI), the itaconate's cell-permeable derivative, can activate Nrf2 signaling via alkylation of Keap1 at its cysteine residues. The current study tested the potential neuroprotective function of OI in hydrogen peroxide (H2O2)-treated neuronal cells.SH-SY5Y neuronal cells and epigenetically de-repressed (by TSA treatment) primary murine neurons were treated with OI and/or H2O2. Nrf2 pathway genes were examined by Western blotting assay and real-time quantitative PCR analysis. Neuronal cell death was tested by the LDH and trypan blue staining assays. Apoptosis was tested by TUNEL and Annexin V assays.In SH-SY5Y neuronal cells and primary murine neurons, OI activated Nrf2 signaling, causing Keap1-Nrf2 disassociation, Nrf2 protein stabilization and nuclear translocation, as well as expression of Nrf2-regulated genes (HO1, NQO1 and GCLC) and ninjurin2 (Ninj2). Functional studies showed that OI attenuated H2O2-induced reactive oxygen species (ROS) production, lipid peroxidation and DNA damage as well as neuronal cell death and apoptosis. shRNA-mediated knockdown, or CRISPR/Cas9-induced knockout of Nrf2 almost abolished OI-induced neuroprotection against H2O2. Keap1 is the primary target of OI. Keap1 knockout by CRISPR/Cas9 method mimicked and abolished OI-induced actions in SH-SY5Y cells. Introduction of a Cys151S mutant Keap1 in SH-SY5Y cells reversed OI-induced Nrf2 activation and anti-H2O2 neuroprotection.OI activates Keap1-Nrf2 signaling to protect SH-SY5Y cells and epigenetically de-repressed primary neurons from H2O2 in vitro.

SH-SY5Y

KEAP1

10.1186/s12964-018-0294-2

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Citations (85)

Cell Adhesion Molecule CD99 in Cancer Immunotherapy

Current Molecular Medicine (2022)

Yu Feng Guodong Liu Hailing Zhang Xiaoyan Wang Zhi Wu

Abstract: The CD99 antigen is a transmembrane protein expressed in a broad variety of tissues, particularly in hematopoietic cells, thymus, endothelial cells, etc. It participates in several crucial biological processes, including cell adhesion, migration, death, differentiation, and inflammation. CD99 has shown oncogenic or tumor suppressor roles in different types of cancer. Therefore, it has been used as a biomarker and therapeutic target for several types of cancer. Moreover, it has also been reported to be involved in several critical immune processes, such as T cell activation and differentiation, dendritic cell differentiation, and so on. Hence, CD99 may have potential values in cancer immunotherapy. Anti-CD99 antibodies have shown therapeutic effects on certain types of cancer, especially on Ewing sarcoma and T cell acute lymphoblastic leukemia (ALL). This review summarizes the recent progress of CD99 in cancer research and targeting therapies, especially in cancer immunotherapy, which may help researchers understand the crucial roles of CD99 in cancer development and design new therapeutic strategies.

CD99

Cancer Immunotherapy

10.2174/1566524023666221007143513

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VTensor: Using Virtual Tensors to Build a Layout-Oblivious AI Programming Framework

2019 IEEE International Conference on Signal, Information and Data Processing (ICSIDP) (2019)

Yu Feng Huimin Cui Xiaobing Feng

With neural networks have achieved great successes in a number of applications such as image classification, visual recognition. Researchers have proposed serval AI programming frameworks such as TensorFlow, Caffe that allows users to train neural network models or deploy them for inference using different accelerate libraries. However, when adding new libraries or new operators to existing frameworks, developers need to spends a lot of effort on layout-dependent code because tensor layout and framework are tightly coupled. Furthermore, inserting a new tuning algorithm into the framework is also difficult. In this paper, we propose VTensor, a novel programming model for developing neural network operators. The key insight is that, layout-dependent can divide into three categories and tuning algorithms have fixed pattern. Specifically, layout-dependent code can split into: accessing tensor information, memory allocation, data preparing and tuning. Based on this observation, we provide layout-oblivious APIs for first and second-class code. For the three-class code, we let developers use description language to describe layout-related information of library, and use code generators to generate dispatch code and tuning code automatically. We evaluate VTensor with a variety of neural network operators in the TensorFlow. Results show that VTensor can effectively decouple the tensor layout from the framework and reduce code size by 50.85% on average. The performance overhead is smaller than 2% with ten typical Convolution Neural Networks (CNNs) execute on Nvidia Titan V.

Code (set theory)

10.1109/icsidp47821.2019.9173314

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The effect of chinese medical psychological sleep regulation technology: a randomized controlled trial for insomnia

Sleep Medicine (2019)

Huaidong Du Li Hong Hongliang Chen Yu Feng Weiming Wang

Sleep

10.1016/j.sleep.2019.11.268

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Chronic TCDD exposure results in the dysregulation of gene expression in splenic B-lymphocytes and in the impairments in T-cell and B-cell differentiation in mouse model

Journal of Environmental Sciences (2016)

Yu Feng Jijing Tian Irina Krylova Tuan Xu Heidi Qunhui Xie

10.1016/j.jes.2015.11.011

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Citations (8)

Gadd45α is involved in regulating activity-dependent and exon-specific BDNF expression in postmitotic cortical neurons

Neuroreport (2021)

Yu Feng Zhen Wang Wei Wei Tingbao Zhang Zhengwei Li

This study aimed to explore the epigenetic regulation of activity-dependent and exon-specific brain-derived neurotrophic factor (BDNF) expression under KCl depolarization in primary cortical neurons.We investigated BDNF exon I, exon IV and the growth arrest and DNA damage-inducible protein 45 alpha (Gadd45α) transcription levels under KCl-induced neuronal activation in postmitotic neurons. Gadd45α occupancy at BDNF I and IV promoter was measured by chromatin immunoprecipitation (ChIP) followed by quantitative PCR; DNA methylation level was checked by methylated DNA immunoprecipitation (MeDIP) followed by qPCR. In addition, lentiviral shRNA targeting Gadd45α was used to knockdown Gadd45α expression.BDNF exon I and IV mRNA expressions were both highly induced by KCl depolarization. However, ChIP analysis demonstrated a significantly increased Gadd45α occupancy only at the BDNF P1 promotor, but not P4, which is associated with reducing DNA methylation within BDNF P1 promoter. Furthermore, after the lentiviral-mediated knockdown of Gadd45α, the increased Gadd45α occupancy at the BDNF P1 was inhibited, which was accompanying the complete blocking of the demethylation effect at P1. Nonetheless, the induction of BDNF exon I mRNA by KCl was only partially prevented by Gadd45α shRNA, indicting other mechanisms involved in regulating BDNF exon I expression.DNA demethylation mediated by Gadd45α protein involves promoting the regulation of activity-dependent BDNF exon I expression in neurons.

Chromatin immunoprecipitation

Gadd45

Methylated DNA immunoprecipitation

DNA demethylation

10.1097/wnr.0000000000001705

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Citations (4)

LncRNA DCRF regulates cardiomyocyte autophagy by targeting miR-551b-5p in diabetic cardiomyopathy

Theranostics (2019)

Yu Feng Weiting Xu Wei Zhang Wenjing Wang Tong Liu

Background: We generated a rat model of diabetic cardiomyopathy (DCM) and reported significant upregulation of the long non-coding RNA DCRF. This study was designed to determine the molecular mechanisms of DCRF in the development of DCM. Methods: Real-time PCR and RNA fluorescent in situ hybridization were conducted to detect the expression pattern of DCRF in cardiomyocytes. Histological and echocardiographic analyses were used to assess the effect of DCRF knockdown on cardiac structure and function in diabetic rats. mRFP-GFP-LC3 fluorescence microscopy, transmission electron microscopy, and Western blotting were carried out to determine cardiomyocyte autophagy. RNA immunoprecipitation and luciferase reporter assays were performed to elucidate the regulatory role of DCRF/miR-551b-5p/PCDH17 pathway in cardiomyocyte autophagy. Results: Our findings showed that DCRF knockdown reduced cardiomyocyte autophagy, attenuated myocardial fibrosis, and improved cardiac function in diabetic rats. High glucose increased DCRF expression and induced autophagy in cardiomyocytes. RNA immunoprecipitation and luciferase reporter assays indicated that DCRF was targeted by miR-551b-5p in an AGO2-dependent manner and PCDH17 was the direct target of miR-551b-5p. Forced expression of DCRF was found to attenuate the inhibitory effect of miR-551b-5p on PCDH17. Furthermore, DCRF knockdown decreased PCDH17 expression and suppressed autophagy in cardiomyocytes treated with high glucose. Conclusion: Our study suggests that DCRF can act as a competing endogenous RNA to increase PCDH17 expression by sponging miR-551b-5p, thus contributing to increased cardiomyocyte autophagy in DCM.

Diabetic Cardiomyopathy

10.7150/thno.31052

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Citations (95)