Xingwang Li

Huazhong Agricultural University

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Guoliang Li

Huazhong Agricultural University

Lin He

West China Medical Center of Sichuan University

Guang He

Shanghai Jiao Tong University

Yifeng Xu

Shanghai Jiao Tong University

Yongyong Shi

Guangzhou University of Chinese Medicine

Guoyin Feng

Shanghai Jiao Tong University

Lun Zhao

Huazhong Agricultural University

Minrong Guo

Huazhong Agricultural University

Zhilin Cao

Henan University of Engineering

Zhiqiang Li

Qingdao University

Cooperative Institutions

Shanghai Jiao Tong University

156

Huazhong Agricultural University

148

Chinese Academy of Sciences

144

Nanjing Medical University

Fudan University

Sun Yat-sen University

Peking University

University of Chinese Academy of Sciences

Chinese Academy of Medical Sciences & Peking Union Medical College

Zhejiang University

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Data from Genome-Wide Association Study of Bladder Cancer in a Chinese Cohort Reveals a New Susceptibility Locus at 5q12.3

Meilin Wang Zhiqiang Li Haiyan Chu Qiang Lv Dingwei Ye

<div>AbstractGenome-wide association studies (GWAS) of bladder cancer have identified a number of susceptibility loci in European populations but have yet to uncover the genetic determinants underlying bladder cancer incidence among other ethnicities. Therefore, we performed the first GWAS in a Chinese cohort comprising 3,406 cases of bladder cancer and 4,645 controls. We identified a new susceptibility locus for bladder cancer at 5q12.3, located in the intron of CWC27 (rs2042329), that was significantly associated with disease risk (OR = 1.40; P = 4.61 × 10−11). However, rs2042329 was not associated with bladder cancer risk in patients of European descent. The rs2042329 risk allele was also related to significantly increased expression levels of CWC27 mRNA and protein in bladder cancer tissues from Chinese patients. Additional functional analyses suggested that CWC27 played an oncogenic role in bladder cancer by inducing cell proliferation and suppressing apoptosis. In conclusion, the identification of a risk-associated locus at 5q12.3 provides new insights into the inherited susceptibility to bladder cancer in Chinese populations and may help to identify high-risk individuals. Cancer Res; 76(11); 3277–84. ©2016 AACR.</div>

Genome-wide Association Study

Genetic predisposition

10.1158/0008-5472.c.6507719

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CTCF-Mediated Human 3D Genome Architecture Reveals Chromatin Topology for Transcription

Cell (2015)

Zhonghui Tang Oscar Junhong Luo Xingwang Li Meizhen Zheng Jacqueline Jufen Zhu

CTCF

Chromosome conformation capture

RNA polymerase II

ChIA-PET

Transcription

Genomic Organization

Pseudoautosomal region

10.1016/j.cell.2015.11.024

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Citations (951)

Technologies for Capturing 3D Genome Architecture in Plants

Trends in Plant Science (2020)

Weizhi Ouyang Qin Xiao Guoliang Li Xingwang Li

Chromosome conformation capture

ChIA-PET

10.1016/j.tplants.2020.10.007

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Citations (9)

Genetic and functional analysis reveals TENM4 contributes to schizophrenia

iScience (2021)

Xin Yi Minzhe Li Guang He Huihui Du Xingwang Li

TENM4, encoding a member of the teneurin protein family, is a risk gene shared by many types of mental diseases and is implicated in neuronal plasticity and signaling. However, the role and the mechanisms of TENM4 in schizophrenia (SCZ) remain unclear. We identified possible pathogenic mutations in the TENM4 gene through target sequencing of TENM4 in 68 SCZ families. We further demonstrated that aberrant expression of Ten-m leads to lower learning ability, sleep reduction, and increased aggressiveness in animal models. RNA sequencing showed that aberrant expression of Ten-m was related to stimulus perception and metabolic process, and Gene Ontology enrichment terms were neurogenesis and ATPase activity. This study provides strong evidence that TENM4 contributes to SCZ, and its functional mutations might be responsible for the impaired neural circuits and behaviors observed in SCZ.

10.1016/j.isci.2021.103063

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Citations (17)

Multiomic Profiling Identifies cis-Regulatory Networks Underlying Human Pancreatic β Cell Identity and Function

Cell Reports (2019)

Nathan Lawlor Eladio J. Márquez Peter Orchard Narisu Narisu Muhammad S. Shamim

EndoC-βH1 is emerging as a critical human β cell model to study the genetic and environmental etiologies of β cell (dys)function and diabetes. Comprehensive knowledge of its molecular landscape is lacking, yet required, for effective use of this model. Here, we report chromosomal (spectral karyotyping), genetic (genotyping), epigenomic (ChIP-seq and ATAC-seq), chromatin interaction (Hi-C and Pol2 ChIA-PET), and transcriptomic (RNA-seq and miRNA-seq) maps of EndoC-βH1. Analyses of these maps define known (e.g., PDX1 and ISL1) and putative (e.g., PCSK1 and mir-375) β cell-specific transcriptional cis-regulatory networks and identify allelic effects on cis-regulatory element use. Importantly, comparison with maps generated in primary human islets and/or β cells indicates preservation of chromatin looping but also highlights chromosomal aberrations and fetal genomic signatures in EndoC-βH1. Together, these maps, and a web application we created for their exploration, provide important tools for the design of experiments to probe and manipulate the genetic programs governing β cell identity and (dys)function in diabetes.

Epigenomics

PDX1

RNA-Seq

Chromosome conformation capture

10.1016/j.celrep.2018.12.083

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Citations (78)

Molecular characterization, expression pattern, and functional analysis of the OsIRL gene family encoding intracellular Ras-group-related LRR proteins in rice

Plant Molecular Biology (2010)

Changjun You Xiaoxia Dai Xingwang Li Lei Wang Guoxing Chen

10.1007/s11103-010-9704-6

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Citations (7)

Probes used for the electrophoretic mobility shift assay.

Yanfang Du Lei Liu Yong Peng Manfei Li Yunfu Li

10.1371/journal.pgen.1008764.s007

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Mapping Multi-Factor-Mediated Chromatin Interactions to Assess Dysregulation of Lung Cancer-Related Genes

Genomics Proteomics & Bioinformatics (2023)

Yan Zhang Jingwen Zhang Wei Zhang Mohan Wang Shuangqi Wang

Abstract Studies on the lung cancer genome are indispensable for developing a cure for lung cancer. Whole-genome resequencing, genome-wide association studies, and transcriptome sequencing have greatly improved our understanding of the cancer genome. However, dysregulation of long-range chromatin interactions in lung cancer remains poorly described. To better understand the three-dimensional (3D) genomic interaction features of the lung cancer genome, we used the A549 cell line as a model system and generated high-resolution chromatin interactions associated with RNA polymerase II (RNAPII), CCCTC-binding factor (CTCF), enhancer of zeste homolog 2 (EZH2), and histone 3 lysine 27 trimethylation (H3K27me3) using long-read chromatin interaction analysis by paired-end tag sequencing (ChIA-PET). Analysis showed that EZH2/H3K27me3-mediated interactions further repressed target genes, either through loops or domains, and their distributions along the genome were distinct from and complementary to those associated with RNAPII. Cancer-related genes were highly enriched with chromatin interactions, and chromatin interactions specific to the A549 cell line were associated with oncogenes and tumor suppressor genes, such as additional repressive interactions on FOXO4 and promoter–promoter interactions between NF1 and RNF135. Knockout of an anchor associated with chromatin interactions reversed the dysregulation of cancer-related genes, suggesting that chromatin interactions are essential for proper expression of lung cancer-related genes. These findings demonstrate the 3D landscape and gene regulatory relationships of the lung cancer genome.

10.1016/j.gpb.2023.01.004

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Citations (1)

Positive association between OLIG2 and schizophrenia in the Chinese Han population

Human Genetics (2007)

Ke Huang Wei Tang Ruqi Tang Xu Zhao Zhangdong He

SNP

OLIG2

Genetic Association

10.1007/s00439-007-0434-z

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Citations (29)

EZH2 contributes to 5-FU resistance in gastric cancer by epigenetically suppressing FBXO32 expression

OncoTargets and Therapy (2018)

Chen‐Yu Wang Xingwang Li Junjie Zhang Zheng Ge Hejin Chen

Background: Increasing evidence suggests the involvement of enhancer of zeste homologue 2 (EZH2) in chemoresistance of cancer treatment. Nevertheless, its function and molecular mechanisms in gastric cancer (GC) chemoresistance are still not well elucidated. Materials and methods: In the present study, we investigated the functional role of EZH2 in 5-fluorouracil (5-FU) resistance of GC cells and discovered the underlying molecular mechanism. Results: Results revealed that EZH2 was upregulated in 5-FU-resistant GC tissues and cell lines. High ZEH2 expression was correlated with poor prognosis of GC patients. EZH2 knockdown enhanced 5-FU sensitivity of AGS/5-FU and SGC-7901/5-FU cells. Moreover, EZH2 could epigenetically suppress FBXO32 expression. FBXO32 overexpression could mimic the functional role of downregulated EZH2 in 5-FU resistance. FBXO32 knockdown counteracted the inductive effect of EZH2 inhibition on 5-FU sensitivity of AGS/5-FU and SGC-7901/5-FU cells. Furthermore, EZH2 knockdown facilitated 5-FU sensitivity of 5-FU-resistant GC cells in vivo. Conclusion: In summary, EZH2 depletion overcame 5-FU resistance in GC by epigenetically silencing FBXO32, providing a novel therapeutic target for GC chemoresistance. Keywords: gastric cancer, 5-FU, enhancer of zeste homologue 2, FBXO32

10.2147/ott.s180131

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Citations (35)