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  1. Article: Editorial: Precision Medicine and Translational Research in Urological Oncology.

    Na, Rong / Olivier, Jonathan / Wei, Gong-Hong

    Frontiers in oncology

    2022  Volume 12, Page(s) 967278

    Language English
    Publishing date 2022-07-05
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2022.967278
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Expanding luminal epitheliums as cells of origin for prostate cancer.

    Gu, Yuexi / Wei, Gong-Hong

    Asian journal of urology

    2020  Volume 8, Issue 2, Page(s) 238–240

    Language English
    Publishing date 2020-10-28
    Publishing country Singapore
    Document type Editorial
    ZDB-ID 2831144-9
    ISSN 2214-3882
    ISSN 2214-3882
    DOI 10.1016/j.ajur.2020.10.003
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  3. Article ; Online: Enhancer Dysfunction in 3D Genome and Disease.

    Xia, Ji-Han / Wei, Gong-Hong

    Cells

    2019  Volume 8, Issue 10

    Abstract: Spatiotemporal patterns of gene expression depend on enhancer elements and other factors during individual development and disease progression. The rapid progress of high-throughput techniques has led to well-defined enhancer chromatin properties. ... ...

    Abstract Spatiotemporal patterns of gene expression depend on enhancer elements and other factors during individual development and disease progression. The rapid progress of high-throughput techniques has led to well-defined enhancer chromatin properties. Various genome-wide methods have revealed a large number of enhancers and the discovery of three-dimensional (3D) genome architecture showing the distant interacting mechanisms of enhancers that loop to target gene promoters. Whole genome sequencing projects directed at cancer have led to the discovery of substantial enhancer dysfunction in misregulating gene expression and in tumor initiation and progression. Results from genome-wide association studies (GWAS) combined with functional genomics analyses have elucidated the functional impacts of many cancer risk-associated variants that are enriched within the enhancer regions of chromatin. Risk variants dysregulate the expression of enhancer variant-associated genes via 3D genomic interactions. Moreover, these enhancer variants often alter the chromatin binding affinity for cancer-relevant transcription factors, which in turn leads to aberrant expression of the genes associated with cancer susceptibility. In this review, we investigate the extent to which these genetic regulatory circuits affect cancer predisposition and how the recent development of genome-editing methods have enabled the determination of the impacts of genomic variation and alteration on cancer phenotype, which will eventually lead to better management plans and treatment responses to human cancer in the clinic.
    MeSH term(s) Animals ; Chromatin/genetics ; Chromatin/metabolism ; Enhancer Elements, Genetic/genetics ; Genetic Predisposition to Disease/genetics ; Genome, Human/genetics ; Genome-Wide Association Study ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Polymorphism, Single Nucleotide/genetics
    Chemical Substances Chromatin
    Language English
    Publishing date 2019-10-19
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells8101281
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  4. Article ; Online: Mechanistic insights into genetic susceptibility to prostate cancer.

    Tian, Pan / Zhong, Mengjie / Wei, Gong-Hong

    Cancer letters

    2021  Volume 522, Page(s) 155–163

    Abstract: Prostate cancer (PCa) is the second most common cancer in men and is a highly heritable disease that affects millions of individuals worldwide. Genome-wide association studies have to date discovered nearly 270 genetic loci harboring hundreds of single ... ...

    Abstract Prostate cancer (PCa) is the second most common cancer in men and is a highly heritable disease that affects millions of individuals worldwide. Genome-wide association studies have to date discovered nearly 270 genetic loci harboring hundreds of single nucleotide polymorphisms (SNPs) that are associated with PCa susceptibility. In contrast, the functional characterization of the mechanisms underlying PCa risk association is still growing. Given that PCa risk-associated SNPs are highly enriched in noncoding cis-regulatory genomic regions, accumulating evidence suggests a widespread modulation of transcription factor chromatin binding and allelic enhancer activity by these noncoding SNPs, thereby dysregulating gene expression. Emerging studies have shown that a proportion of noncoding variants can modulate the formation of transcription factor complexes at enhancers and CTCF-mediated 3D genome architecture. Interestingly, DNA methylation-regulated CTCF binding could orchestrate a long-range chromatin interaction between PCa risk enhancer and causative genes. Additionally, one-causal-variant-two-risk genes or multiple-risk-variant-multiple-genes are prevalent in some PCa risk-associated loci. In this review, we will discuss the current understanding of the general principles of SNP-mediated gene regulation, experimental advances, and functional evidence supporting the mechanistic roles of several PCa genetic loci with potential clinical impact on disease prevention and treatment.
    MeSH term(s) Alleles ; Chromatin/genetics ; DNA Methylation/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Male ; Polymorphism, Single Nucleotide/genetics ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Risk Factors
    Chemical Substances Chromatin
    Language English
    Publishing date 2021-09-22
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2021.09.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  5. Article: Oncogenic regulatory circuits driven by 19q13 rs11672691 underlies prostate cancer aggressiveness.

    Xia, Ji-Han / Wei, Gong-Hong

    Molecular & cellular oncology

    2018  Volume 5, Issue 6, Page(s) e1516451

    Abstract: The 19q13 allele rs11672691 has been reproducibly found in association with aggressive form of prostate cancer, yet the underlying mechanism remains totally unknown. We have recently uncovered a mechanism by which rs11672691 influenced a novel oncogenic ... ...

    Abstract The 19q13 allele rs11672691 has been reproducibly found in association with aggressive form of prostate cancer, yet the underlying mechanism remains totally unknown. We have recently uncovered a mechanism by which rs11672691 influenced a novel oncogenic regulatory circuit, including HOXA2,
    Language English
    Publishing date 2018-09-20
    Publishing country United States
    Document type Journal Article
    ISSN 2372-3556
    ISSN 2372-3556
    DOI 10.1080/23723556.2018.1516451
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  6. Article ; Online: Optimized CRISPR/Cas9-mediated single nucleotide mutation in adherent cancer cell lines.

    Gao, Ping / Dong, Xiaoming / Wang, Yu / Wei, Gong-Hong

    STAR protocols

    2021  Volume 2, Issue 2, Page(s) 100419

    Abstract: CRISPR/Cas9 is an efficient, accurate, and optimizable genome-editing tool. Here, we present a modified CRISPR/Cas9 genome-editing protocol for single nucleotide mutation in adherent cell lines. The protocol was adapted to focus on ease of use and ... ...

    Abstract CRISPR/Cas9 is an efficient, accurate, and optimizable genome-editing tool. Here, we present a modified CRISPR/Cas9 genome-editing protocol for single nucleotide mutation in adherent cell lines. The protocol was adapted to focus on ease of use and efficiency. The protocol here describes how to generate a single nucleotide mutation in cultured 22Rv1 cells. We have also used the protocol in other adherent cell types. Thus, the protocol can be applied to assessing the effect of non-coding single nucleotide polymorphisms (SNPs) in a variety of cell types. For complete details on the use and execution of this protocol, please refer to Gao et al. (2018).
    MeSH term(s) CRISPR-Cas Systems/genetics ; Cell Line, Tumor ; Gene Editing/methods ; Humans ; MCF-7 Cells ; Neoplasms/genetics ; Point Mutation/genetics
    Language English
    Publishing date 2021-03-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2021.100419
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  7. Article: Combined immunotherapy for advanced prostate cancer: Empowering the T cell army.

    Suleman, Sufyan / Wei, Gong-Hong

    Asian journal of urology

    2017  Volume 4, Issue 4, Page(s) 199–200

    Language English
    Publishing date 2017-05-10
    Publishing country Singapore
    Document type Editorial
    ZDB-ID 2831144-9
    ISSN 2214-3882
    ISSN 2214-3882
    DOI 10.1016/j.ajur.2017.04.003
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  8. Article: Combined CRISPRi and proteomics screening reveal a cohesin-CTCF-bound allele contributing to increased expression of

    Tian, Yijun / Dong, Dandan / Wang, Zixian / Wu, Lang / Park, Jong Y / Wei, Gong-Hong / Wang, Liang

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Genome-wide association studies along with expression quantitative trait loci (eQTL) mapping have identified hundreds of single nucleotide polymorphisms (SNPs) and their target genes in prostate cancer (PCa), yet functional characterization of these risk ...

    Abstract Genome-wide association studies along with expression quantitative trait loci (eQTL) mapping have identified hundreds of single nucleotide polymorphisms (SNPs) and their target genes in prostate cancer (PCa), yet functional characterization of these risk loci remains challenging. To screen for potential regulatory SNPs, we designed a CRISPRi library containing 9133 guide RNAs (gRNAs) to target 2,166 candidate SNP sites implicated in PCa and identified 117 SNPs that could regulate 90 genes for PCa cell growth advantage. Among these, rs60464856 was covered by multiple gRNAs significantly depleted in the screening (FDR<0.05). Pooled SNP association analysis in the PRACTICAL and FinnGen cohorts showed significantly higher PCa risk for the rs60464856 G allele (pvalue=1.2E-16 and 3.2E-7). Subsequent eQTL analysis revealed that the G allele is associated with increased
    Language English
    Publishing date 2023-05-10
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.01.18.524405
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  9. Article ; Online: SDC2 Stabilization by USP14 Promotes Gastric Cancer Progression through Co-option of PDK1.

    You, Li / Dou, Yi / Zhang, Yu / Xiao, Hongwei / Lv, Hong / Wei, Gong-Hong / Xu, Dazhi

    International journal of biological sciences

    2023  Volume 19, Issue 11, Page(s) 3483–3498

    Abstract: Gastric cancer (GC) is a common malignancy and remains the fourth-leading cause of cancer-related deaths worldwide. Oncogenic potential of SDC2 has been implicated in multiple types of cancers, yet its role and underlying molecular mechanisms in GC ... ...

    Abstract Gastric cancer (GC) is a common malignancy and remains the fourth-leading cause of cancer-related deaths worldwide. Oncogenic potential of SDC2 has been implicated in multiple types of cancers, yet its role and underlying molecular mechanisms in GC remain unknown. Here, we found that SDC2 was highly expressed in GC and its upregulation correlated with poor prognosis in GC patients. Depletion of SDC2 significantly suppressed the growth and invasive capability of GC cells, while overexpressing SDC2 exerts opposite effects. Combined bioinformatics and experimental analyses substantiated that overexpression of SDC2 activated the AKT signaling pathway in GC, mechanistically through the interaction between SDC2 and PDK1-PH domain, thereby facilitating PDK1 membrane translocation to promote AKT activation. Moreover, SDC2 could also function as a co-receptor for FGF2 and was profoundly involved in the FGF2-AKT signaling axis in GC. Lastly, we revealed a mechanism on the USP14-mediated stabilization of SDC2 that is likely to contribute to SDC2 upregulation in GC tissues. Furthermore, we showed that IU1, a potent USP14 inhibitor, decreased the abundance of SDC2 in GC cells. Our findings indicate that SDC2 functions as a novel GC oncogene and has potential utility as a diagnostic marker and therapeutic target for GC.
    MeSH term(s) Humans ; Cell Line, Tumor ; Cell Proliferation/genetics ; Fibroblast Growth Factor 2/metabolism ; Gene Expression Regulation, Neoplastic ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/genetics ; Stomach Neoplasms/metabolism ; Syndecan-2/metabolism ; Ubiquitin Thiolesterase/metabolism
    Chemical Substances Fibroblast Growth Factor 2 (103107-01-3) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; SDC2 protein, human ; Syndecan-2 (149769-25-5) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; USP14 protein, human ; PDPK1 protein, human (EC 2.7.11.1)
    Language English
    Publishing date 2023-07-09
    Publishing country Australia
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2179208-2
    ISSN 1449-2288 ; 1449-2288
    ISSN (online) 1449-2288
    ISSN 1449-2288
    DOI 10.7150/ijbs.84331
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Genomic Insight into the Role of lncRNA in Cancer Susceptibility.

    Gao, Ping / Wei, Gong-Hong

    International journal of molecular sciences

    2017  Volume 18, Issue 6

    Abstract: With the development of advanced genomic methods, a large amount of long non-coding RNAs (lncRNAs) has been found to be important for cancer initiation and progression. Given that most of the genome-wide association study (GWAS)-identified cancer risk ... ...

    Abstract With the development of advanced genomic methods, a large amount of long non-coding RNAs (lncRNAs) has been found to be important for cancer initiation and progression. Given that most of the genome-wide association study (GWAS)-identified cancer risk SNPs are located in the noncoding region, the expression and function of lncRNAs are more likely to be affected by the SNPs. The SNPs may affect the expression of lncRNAs directly through disrupting the binding of transcription factors or indirectly by affecting the expression of regulatory factors. Moreover, SNPs may disrupt the interaction between lncRNAs and other RNAs or proteins. Unveiling the relationship of lncRNA, protein-coding genes, transcription factors and miRNAs from the angle of genomics will improve the accuracy of disease prediction and help find new therapeutic targets.
    Language English
    Publishing date 2017-06-09
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms18061239
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