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  1. Article ; Online: The Role of p21-Activated Kinases in Cancer and Beyond

    Hui Liu / Kangdong Liu / Zigang Dong

    Frontiers in Cell and Developmental Biology, Vol

    Where Are We Heading?

    2021  Volume 9

    Abstract: The p21-activated kinases (PAKs), downstream effectors of Ras-related Rho GTPase Cdc42 and Rac, are serine/threonine kinases. Biologically, PAKs participate in various cellular processes, including growth, apoptosis, mitosis, immune response, motility, ... ...

    Abstract The p21-activated kinases (PAKs), downstream effectors of Ras-related Rho GTPase Cdc42 and Rac, are serine/threonine kinases. Biologically, PAKs participate in various cellular processes, including growth, apoptosis, mitosis, immune response, motility, inflammation, and gene expression, making PAKs the nexus of several pathogenic and oncogenic signaling pathways. PAKs were proved to play critical roles in human diseases, including cancer, infectious diseases, neurological disorders, diabetes, pancreatic acinar diseases, and cardiac disorders. In this review, we systematically discuss the structure, function, alteration, and molecular mechanisms of PAKs that are involved in the pathogenic and oncogenic effects, as well as PAK inhibitors, which may be developed and deployed in cancer therapy, anti-viral infection, and other diseases. Furthermore, we highlight the critical questions of PAKs in future research, which provide an opportunity to offer input and guidance on new directions for PAKs in pathogenic, oncogenic, and drug discovery research.
    Keywords PAKs ; cancer ; disease ; mechanism ; inhibitor ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2021-03-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Cdc2-like kinases

    Mengqiu Song / Luping Pang / Mengmeng Zhang / Yingzi Qu / Kyle Vaughn Laster / Zigang Dong

    Signal Transduction and Targeted Therapy, Vol 8, Iss 1, Pp 1-

    structure, biological function, and therapeutic targets for diseases

    2023  Volume 25

    Abstract: Abstract The CLKs (Cdc2-like kinases) belong to the dual-specificity protein kinase family and play crucial roles in regulating transcript splicing via the phosphorylation of SR proteins (SRSF1–12), catalyzing spliceosome molecular machinery, and ... ...

    Abstract Abstract The CLKs (Cdc2-like kinases) belong to the dual-specificity protein kinase family and play crucial roles in regulating transcript splicing via the phosphorylation of SR proteins (SRSF1–12), catalyzing spliceosome molecular machinery, and modulating the activities or expression of non-splicing proteins. The dysregulation of these processes is linked with various diseases, including neurodegenerative diseases, Duchenne muscular dystrophy, inflammatory diseases, viral replication, and cancer. Thus, CLKs have been considered as potential therapeutic targets, and significant efforts have been exerted to discover potent CLKs inhibitors. In particular, clinical trials aiming to assess the activities of the small molecules Lorecivivint on knee Osteoarthritis patients, and Cirtuvivint and Silmitasertib in different advanced tumors have been investigated for therapeutic usage. In this review, we comprehensively documented the structure and biological functions of CLKs in various human diseases and summarized the significance of related inhibitors in therapeutics. Our discussion highlights the most recent CLKs research, paving the way for the clinical treatment of various human diseases.
    Keywords Medicine ; R ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2023-04-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Pairing Cancer Biomarkers to Biomedicine

    Seung Ho Shin / Zigang Dong

    EBioMedicine, Vol 25, Iss C, Pp 1-

    2017  Volume 2

    Keywords Medicine ; R ; Medicine (General) ; R5-920
    Language English
    Publishing date 2017-11-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Visualization of two architectures in class-II CAP-dependent transcription activation.

    Wei Shi / Yanan Jiang / Yibin Deng / Zigang Dong / Bin Liu

    PLoS Biology, Vol 18, Iss 4, p e

    2020  Volume 3000706

    Abstract: Transcription activation by cyclic AMP (cAMP) receptor protein (CAP) is the classic paradigm of transcription regulation in bacteria. CAP was suggested to activate transcription on class-II promoters via a recruitment and isomerization mechanism. However, ...

    Abstract Transcription activation by cyclic AMP (cAMP) receptor protein (CAP) is the classic paradigm of transcription regulation in bacteria. CAP was suggested to activate transcription on class-II promoters via a recruitment and isomerization mechanism. However, whether and how it modifies RNA polymerase (RNAP) to initiate transcription remains unclear. Here, we report cryo-electron microscopy (cryo-EM) structures of an intact Escherichia coli class-II CAP-dependent transcription activation complex (CAP-TAC) with and without de novo RNA transcript. The structures reveal two distinct architectures of TAC and raise the possibility that CAP binding may induce substantial conformational changes in all the subunits of RNAP and transiently widen the main cleft of RNAP to facilitate DNA promoter entering and formation of the initiation open complex. These structural changes vanish during further RNA transcript synthesis. The observations in this study may reveal a possible on-pathway intermediate and suggest a possibility that CAP activates transcription by inducing intermediate state, in addition to the previously proposed stabilization mechanism.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2020-04-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Acetylshikonin inhibits inflammatory responses and Papain-like protease activity in murine model of COVID-19

    Ning Lu / Tingxuan Gu / Xueli Tian / Simin Zhao / Guoguo Jin / Fredimoses Mangaladoss / Yan Qiao / Kangdong Liu / Ran Zhao / Zigang Dong

    Signal Transduction and Targeted Therapy, Vol 7, Iss 1, Pp 1-

    2022  Volume 3

    Keywords Medicine ; R ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2022-10-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Crystal structure of the human PRPK–TPRKB complex

    Jian Li / Xinli Ma / Surajit Banerjee / Hanyong Chen / Weiya Ma / Ann M. Bode / Zigang Dong

    Communications Biology, Vol 4, Iss 1, Pp 1-

    2021  Volume 11

    Abstract: Jian Li and Xinli Ma et al. present a 2.53 Å crystal structure of a complex consisting of the human p53-related protein kinase (PRPK), TP53RK-binding protein, and adenylyl-imidodiphosphate. They find that one disease mutation, PRPK K238Nfs*2, is ... ...

    Abstract Jian Li and Xinli Ma et al. present a 2.53 Å crystal structure of a complex consisting of the human p53-related protein kinase (PRPK), TP53RK-binding protein, and adenylyl-imidodiphosphate. They find that one disease mutation, PRPK K238Nfs*2, is important for PRPK’s binding to O-sialoglycoprotein endopeptidase, providing insights into rational drug design.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-02-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Spatial transcriptomics analysis of esophageal squamous precancerous lesions and their progression to esophageal cancer

    Xuejiao Liu / Simin Zhao / Keke Wang / Liting Zhou / Ming Jiang / Yunfeng Gao / Ran Yang / Shiwen Yan / Wen Zhang / Bingbing Lu / Feifei Liu / Ran Zhao / Wenting Liu / Zihan Zhang / Kangdong Liu / Xiang Li / Zigang Dong

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Volume 20

    Abstract: Abstract Esophageal squamous precancerous lesions (ESPL) are the precursors of esophageal squamous cell carcinoma (ESCC) including low-grade and high-grade intraepithelial neoplasia. Due to the absence of molecular indicators, which ESPL will eventually ... ...

    Abstract Abstract Esophageal squamous precancerous lesions (ESPL) are the precursors of esophageal squamous cell carcinoma (ESCC) including low-grade and high-grade intraepithelial neoplasia. Due to the absence of molecular indicators, which ESPL will eventually develop into ESCC and thus should be treated is not well defined. Indicators, for predicting risks of ESCC at ESPL stages, are an urgent need. We perform spatial whole-transcriptome atlas analysis, which can eliminate other tissue interference by sequencing the specific ESPL regions. In this study, the expression of TAGLN2 significantly increases, while CRNN expression level decreases along the progression of ESCC. Additionally, TAGLN2 protein level significantly increases in paired after-progression tissues compared with before-progression samples, while CRNN expression decreases. Functional studies suggest that TAGLN2 promotes ESCC progression, while CRNN inhibits it by regulating cell proliferation. Taken together, TAGLN2 and CRNN are suggested as candidate indicators for the risk of ESCC at ESPL stages.
    Keywords Science ; Q
    Language English
    Publishing date 2023-08-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Four Is Better Than 1—Strength in Numbers!

    Ann M. Bode, Ph.D. / Zigang Dong, M.D., Dr. P.H.

    EBioMedicine, Vol 11, Iss C, Pp 17-

    2016  Volume 18

    Keywords Medicine ; R ; Medicine (General) ; R5-920
    Language English
    Publishing date 2016-09-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Targeting integrin αvβ3 with indomethacin inhibits patient‐derived xenograft tumour growth and recurrence in oesophageal squamous cell carcinoma

    Fangfang Liu / Qiong Wu / Wei Han / Kyle Laster / Yamei Hu / Fayang Ma / Hanyong Chen / Xueli Tian / Yan Qiao / Hui Liu / Dong Joon Kim / Zigang Dong / Kangdong Liu

    Clinical and Translational Medicine, Vol 11, Iss 10, Pp n/a-n/a (2021)

    2021  

    Abstract: Abstract Rationale A high risk of post‐operative recurrence contributes to the poor prognosis and low survival rate of oesophageal squamous cell carcinoma (ESCC) patients. Increasing experimental evidence suggests that integrin adhesion receptors, in ... ...

    Abstract Abstract Rationale A high risk of post‐operative recurrence contributes to the poor prognosis and low survival rate of oesophageal squamous cell carcinoma (ESCC) patients. Increasing experimental evidence suggests that integrin adhesion receptors, in particular integrin αv (ITGAV), are important for cancer cell survival, proliferation and migration. Therefore, targeting ITGAV may be a rational approach for preventing ESCC recurrence. Materials and methods Protein levels of ITGAV were determined in human ESCC tumour tissues using immunohistochemistry. MTT, propidium iodide staining, and annexin V staining were utilized to investigate cell viability, cell cycle progression, and induction of apoptosis, respectively. Computational docking was performed with the Schrödinger Suite software to visualize the interaction between indomethacin and ITGAV. Cell‐derived xenograft mouse models, patient‐derived xenograft (PDX) mouse models, and a humanized mouse model were employed for in vivo studies. Results ITGAV was upregulated in human ESCC tumour tissues and increased ITGAV protein levels were associated with poor prognosis. ITGAV silencing or knockout suppressed ESCC cell growth and metastatic potential. Interestingly, we identified that indomethacin can bind to ITGAV and enhance synovial apoptosis inhibitor 1 (SYVN1)‐mediated degradation of ITGAV. Integrin β3, one of the β subunits of ITGAV, was also decreased at the protein level in the indomethacin treatment group. Importantly, indomethacin treatment suppressed ESCC tumour growth and prevented recurrence in a PDX mouse model. Moreover, indomethacin inhibited the activation of cytokine TGFβ, reduced SMAD2/3 phosphorylation, and increased anti‐tumour immune responses in a humanized mouse model. Conclusion ITGAV is a promising therapeutic target for ESCC. Indomethacin can attenuate ESCC growth through binding to ITGAV, promoting SYVN1‐mediated ubiquitination of ITGAV, and potentiating cytotoxic CD8+ T cell responses.
    Keywords ESCC ; indomethacin ; integrin αvβ3 ; recurrence ; Medicine (General) ; R5-920
    Subject code 616
    Language English
    Publishing date 2021-10-01T00:00:00Z
    Publisher Wiley
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: 3-Deoxysappanchalcone Inhibits Skin Cancer Proliferation by Regulating T-Lymphokine-Activated Killer Cell-Originated Protein Kinase in vitro and in vivo

    Xiaorong Fu / Ran Zhao / Goo Yoon / Jung-Hyun Shim / Bu Young Choi / Fanxiang Yin / Beibei Xu / Kyle Vaughn Laster / Kangdong Liu / Zigang Dong / Mee-Hyun Lee

    Frontiers in Cell and Developmental Biology, Vol

    2021  Volume 9

    Abstract: BackgroundSkin cancer is one of the most commonly diagnosed cancers worldwide. The 5-year survival rate of the most aggressive late-stage skin cancer ranges between 20 and 30%. Thus, the discovery and investigation of novel target therapeutic agents that ...

    Abstract BackgroundSkin cancer is one of the most commonly diagnosed cancers worldwide. The 5-year survival rate of the most aggressive late-stage skin cancer ranges between 20 and 30%. Thus, the discovery and investigation of novel target therapeutic agents that can effectively treat skin cancer is of the utmost importance. The T-lymphokine-activated killer cell-originated protein kinase (TOPK), which belongs to the serine-threonine kinase class of the mitogen-activated protein kinase kinase (MAPKK) family, is highly expressed and activated in skin cancer. The present study investigates the role of 3-deoxysappanchalcone (3-DSC), a plant-derived functional TOPK inhibitor, in suppressing skin cancer cell growth.PurposeIn the context of skin cancer prevention and therapy, we clarify the effect and mechanism of 3-DSC on different types of skin cancer and solar-simulated light (SSL)-induced skin hyperplasia.MethodsIn an in vitro study, western blotting and in vitro kinase assays were utilized to determine the protein expression of TOPK and its activity, respectively. Pull-down assay with 3-DSC and TOPK (wild-type and T42A/N172 mutation) was performed to confirm the direct interaction between T42A/N172 amino acid sites of TOPK and 3-DSC. Cell proliferation and anchorage-independent cell growth assays were utilized to determine the effect of 3-DSC on cell growth. In an in vivo study, the thickness of skin and tumor size were measured in the acute SSL-induced inflammation mouse model or SK-MEL-2 cell-derived xenografts mouse model treated with 3-DSC. Immunohistochemistry analysis of tumors isolated from SK-MEL-2 cell-derived xenografts was performed to determine whether cell-based results observed upon 3-DSC treatment could be recapitulated in vivo.Results3-DSC is able to inhibit cell proliferation in skin cancer cells in an anchorage-dependent and anchorage-independent manner by regulation of TOPK and its related signaling pathway in vitro. We also found that application of 3-DSC reduced acute SSL-induced murine skin ...
    Keywords skin cancer ; solar sinulated light ; T-LAK cell-originated protein kinase ; 3-deoxysappanchalcone ; cancer growth ; skin hyperplasia ; Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2021-03-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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