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  1. Article ; Online: RIOK1 mediates p53 degradation and radioresistance in colorectal cancer through phosphorylation of G3BP2.

    Chen, Yaqi / Zhou, Sha / Wan, Kairui / Yu, Long / Zhao, Chongchong / Deng, Haiteng / Ou, Qingjian / Qin, Jiayi / Hu, Junbo / Hou, Zhenlin

    Oncogene

    2022  Volume 41, Issue 25, Page(s) 3433–3444

    Abstract: RIO Kinase 1 (RIOK1) is involved in various pathologies, including cancer. However, the role of RIOK1 in radioresistance of colorectal cancer (CRC) remains largely unknown. In this study, we reported that RIOK1 was overexpressed in rectal cancer tissue ... ...

    Abstract RIO Kinase 1 (RIOK1) is involved in various pathologies, including cancer. However, the role of RIOK1 in radioresistance of colorectal cancer (CRC) remains largely unknown. In this study, we reported that RIOK1 was overexpressed in rectal cancer tissue with weaker tumor regression after neoadjuvant chemoradiotherapy (neoCRT). Moreover, higher RIOK1 expression predicted a poor prognosis in patients with rectal cancer. Blockade of RIOK1 using Toyocamycin, a pharmacological inhibitor of RIOK1, or by knocking down its expression, decreased the resistance of CRC cells to radiotherapy in vitro and in vivo. A mechanistic study revealed that RIOK1 regulates radioresistance by suppressing the p53 signaling pathway. Furthermore, we found that RIOK1 and Ras-GAP SH3 domain binding protein 2 (G3BP2) interact with each other. RIOK1 phosphorylates G3BP2 at Thr226, which increases the activity of G3BP2. RIOK1-mediated phosphorylation of G3BP2 facilitated ubiquitination of p53 by murine double minute 2 protein (MDM2). Altogether, our study revealed the clinical significance of RIOK1 in CRC, and therapies targeting RIOK1 might alleviate the CRC tumor burden in patients.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Line, Tumor ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/radiotherapy ; Humans ; Mice ; Phosphorylation ; Protein Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-mdm2/metabolism ; RNA-Binding Proteins/metabolism ; Rectal Neoplasms ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; G3BP2 protein, human ; RNA-Binding Proteins ; Tumor Suppressor Protein p53 ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; RIOK1 protein, human (EC 2.7.11.1)
    Language English
    Publishing date 2022-05-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-022-02352-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: NSD2 methylates AROS to promote SIRT1 activation and regulates fatty acid metabolism-mediated cancer radiotherapy.

    Li, Xun / Song, Da / Chen, Yaqi / Huang, Changsheng / Liu, Anyi / Wu, Qi / She, Xiaowei / Li, Kangdi / Wan, Kairui / Yu, Chengxin / Qiu, Cheng / Liu, Lang / Wang, Guihua / Xu, Feng / Wang, Jing / Hu, Junbo

    Cell reports

    2023  Volume 42, Issue 10, Page(s) 113126

    Abstract: Fatty acid metabolism plays a critical role in both tumorigenesis and cancer radiotherapy. However, the regulatory mechanism of fatty acid metabolism has not been fully elucidated. NSD2, a histone methyltransferase that catalyzes di-methylation of ... ...

    Abstract Fatty acid metabolism plays a critical role in both tumorigenesis and cancer radiotherapy. However, the regulatory mechanism of fatty acid metabolism has not been fully elucidated. NSD2, a histone methyltransferase that catalyzes di-methylation of histone H3 at lysine 36, has been shown to play an essential role in tumorigenesis and cancer progression. Here, we show that NSD2 promotes fatty acid oxidation (FAO) by methylating AROS (active regulator of SIRT1) at lysine 27, facilitating the physical interaction between AROS and SIRT1. The mutation of lysine 27 to arginine weakens the interaction between AROS and SIRT1 and impairs AROS-SIRT1-mediated FAO. Additionally, we examine the effect of NSD2 inhibition on radiotherapy efficacy and find an enhanced effectiveness of radiotherapy. Together, our findings identify a NSD2-dependent methylation regulation pattern of the AROS-SIRT1 axis, suggesting that NSD2 inhibition may be a potential adjunct for tumor radiotherapy.
    MeSH term(s) Humans ; Sirtuin 1/genetics ; Repressor Proteins/metabolism ; Lysine/metabolism ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Neoplasms/genetics ; Neoplasms/radiotherapy ; Carcinogenesis ; Fatty Acids
    Chemical Substances Sirtuin 1 (EC 3.5.1.-) ; Repressor Proteins ; Lysine (K3Z4F929H6) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; Fatty Acids ; SIRT1 protein, human (EC 3.5.1.-)
    Language English
    Publishing date 2023-09-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.113126
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Inhibition of CARM1-Mediated Methylation of ACSL4 Promotes Ferroptosis in Colorectal Cancer.

    Feng, Shengjie / Rao, Zejun / Zhang, Jiakun / She, Xiaowei / Chen, Yaqi / Wan, Kairui / Li, Haijie / Zhao, Chongchong / Feng, Yongdong / Wang, Guihua / Hu, Junbo / Luo, Xuelai

    Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    2023  Volume 10, Issue 36, Page(s) e2303484

    Abstract: Ferroptosis, which is caused by iron-dependent accumulation of lipid peroxides, is an emerging form of regulated cell death and is considered a potential target for cancer therapy. However, the regulatory mechanisms underlying ferroptosis remain unclear. ...

    Abstract Ferroptosis, which is caused by iron-dependent accumulation of lipid peroxides, is an emerging form of regulated cell death and is considered a potential target for cancer therapy. However, the regulatory mechanisms underlying ferroptosis remain unclear. This study defines a distinctive role of ferroptosis. Inhibition of CARM1 can increase the sensitivity of tumor cells to ferroptosis inducers in vitro and in vivo. Mechanistically, it is found that ACSL4 is methylated by CARM1 at arginine 339 (R339). Furthermore, ACSL4 R339 methylation promotes RNF25 binding to ACSL4, which contributes to the ubiquitylation of ACSL4. The blockade of CARM1 facilitates ferroptosis and effectively enhances ferroptosis-associated cancer immunotherapy. Overall, this study demonstrates that CARM1 is a critical contributor to ferroptosis resistance and highlights CARM1 as a candidate therapeutic target for improving the effects of ferroptosis-based antitumor therapy.
    MeSH term(s) Humans ; Ferroptosis ; Methylation ; Protein-Arginine N-Methyltransferases/genetics ; Colorectal Neoplasms/genetics
    Chemical Substances coactivator-associated arginine methyltransferase 1 (EC 2.1.1.319) ; Protein-Arginine N-Methyltransferases (EC 2.1.1.319)
    Language English
    Publishing date 2023-11-09
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2808093-2
    ISSN 2198-3844 ; 2198-3844
    ISSN (online) 2198-3844
    ISSN 2198-3844
    DOI 10.1002/advs.202303484
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Quality changes of clinical practice guidelines for respiratory diseases in China: A systematic review.

    Wan, Kai-Rui / Zeng, Guang-Qiao / Li, Yao / Wu, Jun-Wan / Zou, Bang-Yu / Liang, Heng-Rui / Jiang, Mei

    The clinical respiratory journal

    2021  Volume 15, Issue 9, Page(s) 983–991

    Abstract: Background: After the low quality of Chinese clinical practice guidelines (CPGs) for respiratory diseases published from 1979 to 2013 was reported, some handbooks were published to standardize guidelines' development recently. There was a great increase ...

    Abstract Background: After the low quality of Chinese clinical practice guidelines (CPGs) for respiratory diseases published from 1979 to 2013 was reported, some handbooks were published to standardize guidelines' development recently. There was a great increase in the production and dissemination of CPGs annually in China, whose quality and potential impact were unknown.
    Methods: A systematic search of four literature databases was performed for the period January 2013 to December 2018 to identify Chinese CPGs for respiratory diseases. Eligible CPGs were evaluated using the appraisal of guidelines for research and evaluation II (AGREE II) instrument.
    Results: A total of 197 CPGs were identified for review. Compared with the result of previous study, the increased scores of the six AGREE II domains were screened: Scope and purpose (57.3% vs. 57.8%), Stakeholder involvement (17.6% vs. 25.0%), Rigor of development (10.2% vs. 13.2%), Clarity and presentation (55.2% vs. 58.4%), Applicability (9.3% vs. 25.9%), and Editorial independence (1.1% vs. 6.3%). The improved overall assessment for included CPGs were: Recommended (4, 2.0% vs. 0, 0%) and Recommended with modifications (26, 13.2% vs. 3, 2.8%). The improved level of evidence used to make recommendations were 59, 11.9% versus 168, 22.4% and 88, 17.7% versus 195, 26.0%, A and B, respectively.
    Conclusions: The overall quality of CPGs for respiratory diseases published from 2013 to 2018 in China was slightly improved, but had a big gap with the optimum level, especially in Rigor of development and Editorial independence. Increased efforts are required to enable the development of high-quality evidence-based CPGs for respiratory diseases.
    MeSH term(s) China/epidemiology ; Databases, Factual ; Humans ; Practice Guidelines as Topic
    Language English
    Publishing date 2021-06-13
    Publishing country England
    Document type Journal Article ; Systematic Review
    ZDB-ID 2442214-9
    ISSN 1752-699X ; 1752-6981
    ISSN (online) 1752-699X
    ISSN 1752-6981
    DOI 10.1111/crj.13402
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: SETDB1 Methylates MCT1 Promoting Tumor Progression by Enhancing the Lactate Shuttle.

    She, Xiaowei / Wu, Qi / Rao, Zejun / Song, Da / Huang, Changsheng / Feng, Shengjie / Liu, Anyi / Liu, Lang / Wan, Kairui / Li, Xun / Yu, Chengxin / Qiu, Cheng / Luo, Xuelai / Hu, Junbo / Wang, Guihua / Xu, Feng / Sun, Li

    Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    2023  Volume 10, Issue 28, Page(s) e2301871

    Abstract: MCT1 is a critical protein found in monocarboxylate transporters that plays a significant role in regulating the lactate shuttle. However, the post-transcriptional modifications that regulate MCT1 are not clearly identified. In this study, it is reported ...

    Abstract MCT1 is a critical protein found in monocarboxylate transporters that plays a significant role in regulating the lactate shuttle. However, the post-transcriptional modifications that regulate MCT1 are not clearly identified. In this study, it is reported that SETDB1 interacts with MCT1, leading to its stabilization. These findings reveal a novel post-translational modification of MCT1, in which SETDB1 methylation occurs at K473 in vitro and in vivo. This methylation inhibits the interaction between MCT1 and Tollip, which blocks Tollip-mediated autophagic degradation of MCT1. Furthermore, MCT1 K473 tri-methylation promotes tumor glycolysis and M2-like polarization of tumor-associated macrophages in colorectal cancer (CRC), which enhances the lactate shuttle. In clinical studies, MCT1 K473 tri-methylation is found to be upregulated and positively correlated with tumor progression and overall survival in CRC. This discovery suggests that SETDB1-mediated tri-methylation at K473 is a vital regulatory mechanism for lactate shuttle and tumor progression. Additionally, MCT1 K473 methylation may be a potential prognostic biomarker and promising therapeutic target for CRC.
    MeSH term(s) Humans ; Lactic Acid/metabolism ; Symporters ; Neoplasms ; Histone-Lysine N-Methyltransferase/metabolism
    Chemical Substances Lactic Acid (33X04XA5AT) ; Symporters ; SETDB1 protein, human (EC 2.1.1.43) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
    Language English
    Publishing date 2023-08-04
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2808093-2
    ISSN 2198-3844 ; 2198-3844
    ISSN (online) 2198-3844
    ISSN 2198-3844
    DOI 10.1002/advs.202301871
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: A quality assessment of evidence-based guidelines for the prevention and management of ventilator-associated pneumonia: a systematic review.

    Wan, Kairui / Liang, Hengrui / Yan, Guolin / Zou, Bangyu / Huang, Chuxin / Jiang, Mei

    Journal of thoracic disease

    2018  Volume 11, Issue 7, Page(s) 2795–2807

    Abstract: Background: Numerous evidence-based guidelines (EBGs) pertaining to ventilator-associated pneumonia (VAP) have been published by domestic and international organizations, but their qualities have not been reported.: Methods: A systematic search of ... ...

    Abstract Background: Numerous evidence-based guidelines (EBGs) pertaining to ventilator-associated pneumonia (VAP) have been published by domestic and international organizations, but their qualities have not been reported.
    Methods: A systematic search of the literature was performed up to July 2018 for relevant guidelines. Guidelines were eligible for inclusion if they incorporated recommendation statements for prevention and/or management in adults or children with VAP and were developed on a systematic evidence-based method. Four reviewers evaluated each guideline using the Appraisal of Guidelines for Research and Evaluation II (AGREE II) instrument, which comprises 23 items organized into six domains in addition to two overall items.
    Results: Thirteen EBGs were identified for review. An overall high degree of agreement among reviewers was reached [intra-class correlation coefficient (ICC), 0.885; 95% CI, 0.862-0.905] during their review. The scores (mean, range) for the six AGREE domains were:
    Conclusions: The overall quality of the identified EBGs pertaining to VAP was classified as moderate. The management of VAP varied by guideline. More high-quality evidence is needed to improve guideline recommendations.
    Language English
    Publishing date 2018-07-16
    Publishing country China
    Document type Journal Article
    ZDB-ID 2573571-8
    ISSN 2077-6624 ; 2072-1439
    ISSN (online) 2077-6624
    ISSN 2072-1439
    DOI 10.21037/jtd.2019.06.56
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: PRMT5 methylating SMAD4 activates TGF-β signaling and promotes colorectal cancer metastasis.

    Liu, Anyi / Yu, Chengxin / Qiu, Cheng / Wu, Qi / Huang, Changsheng / Li, Xun / She, Xiaowei / Wan, Kairui / Liu, Lang / Li, Mao / Wang, Zhihong / Chen, Yaqi / Hu, Fuqing / Song, Da / Li, Kangdi / Zhao, Chongchong / Deng, Haiteng / Sun, Xuling / Xu, Feng /
    Lai, Senyan / Luo, Xuelai / Hu, Junbo / Wang, Guihua

    Oncogene

    2023  Volume 42, Issue 19, Page(s) 1572–1584

    Abstract: Perturbations in transforming growth factor-β (TGF-β) signaling can lead to a plethora of diseases, including cancer. Mutations and posttranslational modifications (PTMs) of the partner of SMAD complexes contribute to the dysregulation of TGF-β signaling. ...

    Abstract Perturbations in transforming growth factor-β (TGF-β) signaling can lead to a plethora of diseases, including cancer. Mutations and posttranslational modifications (PTMs) of the partner of SMAD complexes contribute to the dysregulation of TGF-β signaling. Here, we reported a PTM of SMAD4, R361 methylation, that was critical for SMAD complexes formation and TGF-β signaling activation. Through mass spectrometric, co-immunoprecipitation (Co-IP) and immunofluorescent (IF) assays, we found that oncogene protein arginine methyltransferase 5 (PRMT5) interacted with SMAD4 under TGF-β1 treatment. Mechanically, PRMT5 triggered SMAD4 methylation at R361 and induced SMAD complexes formation and nuclear import. Furthermore, we emphasized that PRMT5 interacting and methylating SMAD4 was required for TGF-β1-induced epithelial-mesenchymal transition (EMT) and colorectal cancer (CRC) metastasis, and SMAD4 R361 mutation diminished PRMT5 and TGF-β1-induced metastasis. In addition, highly expressed PRMT5 or high level of SMAD4 R361 methylation indicated worse outcomes in clinical specimens analysis. Collectively, our study highlights the critical interaction of PRMT5 and SMAD4 and the roles of SMAD4 R361 methylation for controlling TGF-β signaling during metastasis. We provided a new insight for SMAD4 activation. And this study indicated that blocking PRMT5-SMAD4 signaling might be an effective targeting strategy in SMAD4 wild-type CRC.
    MeSH term(s) Humans ; Cell Line, Tumor ; Colorectal Neoplasms/pathology ; Protein-Arginine N-Methyltransferases/genetics ; Protein-Arginine N-Methyltransferases/metabolism ; Signal Transduction ; Smad4 Protein/genetics ; Smad4 Protein/metabolism ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta1/metabolism ; Neoplasm Metastasis
    Chemical Substances PRMT5 protein, human (EC 2.1.1.319) ; Protein-Arginine N-Methyltransferases (EC 2.1.1.319) ; Smad4 Protein ; SMAD4 protein, human ; Transforming Growth Factor beta ; Transforming Growth Factor beta1
    Language English
    Publishing date 2023-03-29
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-023-02674-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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