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  1. Article ; Online: Editorial: Epigenetic, metabolic, and transcriptional regulation of immune cell plasticity and functions in cancer and non-cancer diseases.

    Dai, Yun / Ren, Dong / He, Yafeng / Yi, Huanfa

    Frontiers in immunology

    2023  Volume 14, Page(s) 1284124

    MeSH term(s) Humans ; Cell Plasticity ; Neoplasms/genetics ; Gene Expression Regulation ; Biochemical Phenomena ; Epigenesis, Genetic
    Language English
    Publishing date 2023-09-25
    Publishing country Switzerland
    Document type Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1284124
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Corrigendum: Identifying neutrophil-associated subtypes in ulcerative colitis and confirming neutrophils promote colitis-associated colorectal cancer.

    Zhang, Chen / Zhang, Jiantao / Zhang, Yanli / Song, Zian / Bian, Jing / Yi, Huanfa / Ma, Zhanchuan

    Frontiers in immunology

    2024  Volume 15, Page(s) 1376797

    Abstract: This corrects the article DOI: 10.3389/fimmu.2023.1095098.]. ...

    Abstract [This corrects the article DOI: 10.3389/fimmu.2023.1095098.].
    Language English
    Publishing date 2024-04-10
    Publishing country Switzerland
    Document type Published Erratum
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2024.1376797
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Long Noncoding RNAs as Orchestrators of CD4

    Liu, Chang / Zhang, Yanli / Ma, Zhanchuan / Yi, Huanfa

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 831215

    Abstract: ... ...

    Abstract CD4
    Language English
    Publishing date 2022-06-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.831215
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The dysregulation of lncRNAs by epigenetic factors in human pathologies.

    Zhang, Yanli / Wang, Xiaocong / Zhang, Chen / Yi, Huanfa

    Drug discovery today

    2023  Volume 28, Issue 9, Page(s) 103664

    Abstract: Dysregulation of long noncoding RNAs (lncRNAs) contributes to numerous human diseases, including cancers and autoimmune diseases (ADs). Given the importance of lncRNAs in disease initiation and progression, a deeper understanding of their complex ... ...

    Abstract Dysregulation of long noncoding RNAs (lncRNAs) contributes to numerous human diseases, including cancers and autoimmune diseases (ADs). Given the importance of lncRNAs in disease initiation and progression, a deeper understanding of their complex regulatory network is required to facilitate their use as therapeutic targets for ADs. In this review, we summarize how lncRNAs are dysregulated in pathological states by epigenetic factors, including RNA-binding proteins, chemical modifications (N6-methyladenosine, 5-methylcytosine, 7-methylguanosine, adenosine-to-inosine editing, microRNA, alternative splicing, DNA methylation, and histone modification). Moreover, the roles of lncRNA epigenetic regulators in immune response and ADs are discussed, providing new insights into the complicated epigenetic factor-lncRNA network, thus, laying a theoretical foundation for future research and clinical application of lncRNAs.
    MeSH term(s) Humans ; RNA, Long Noncoding/metabolism ; DNA Methylation ; MicroRNAs ; Adenosine ; Epigenesis, Genetic
    Chemical Substances RNA, Long Noncoding ; MicroRNAs ; Adenosine (K72T3FS567)
    Language English
    Publishing date 2023-06-20
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1324988-5
    ISSN 1878-5832 ; 1359-6446
    ISSN (online) 1878-5832
    ISSN 1359-6446
    DOI 10.1016/j.drudis.2023.103664
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4725: Show issues Location:
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  5. Article ; Online: Shiny transcriptional junk: lncRNA-derived peptides in cancers and immune responses.

    Zhang, Yanli / Wang, Xiaocong / Hu, Cong / Yi, Huanfa

    Life sciences

    2023  Volume 316, Page(s) 121434

    Abstract: By interacting with DNA, RNA, and proteins, long noncoding RNAs (lncRNAs) have been linked to several pathological states. LncRNA-derived peptides, as a novel modality of action of lncRNAs, have recently become a research hotspot. An increasing body of ... ...

    Abstract By interacting with DNA, RNA, and proteins, long noncoding RNAs (lncRNAs) have been linked to several pathological states. LncRNA-derived peptides, as a novel modality of action of lncRNAs, have recently become a research hotspot. An increasing body of evidence has demonstrated the important role of these peptides in carcinogenesis and cancer progression and immune response. This review first describes lncRNA-derived peptides, the regulators that control their translation, and the roles of these peptides in multiple biological processes and disease states including cancers. In the following section, we comprehensively analyzed the significant role lncRNA-derived peptide played in the immune response. This review provides fresh perspectives on the biological role of lncRNAs and their relationship with diseases, particularly with cancers and the immune response, providing a theoretical basis for these lncRNA-derived peptides as therapeutic and diagnostic targets in cancers and inflammatory diseases.
    MeSH term(s) Humans ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Carcinogenesis ; Immunity ; Peptides/genetics
    Chemical Substances RNA, Long Noncoding ; Peptides
    Language English
    Publishing date 2023-01-24
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2023.121434
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.368: Show issues Location:
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  6. Article: SLC2As

    Zhang, Yanli / Qin, Han / Bian, Jing / Ma, Zhanchuan / Yi, Huanfa

    Frontiers in pharmacology

    2022  Volume 13, Page(s) 1045179

    Abstract: Facilitative glucose transporters (GLUTs), which are encoded by solute carrier 2A ( ...

    Abstract Facilitative glucose transporters (GLUTs), which are encoded by solute carrier 2A (
    Language English
    Publishing date 2022-11-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2022.1045179
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Shiny transcriptional junk: lncRNA-derived peptides in cancers and immune responses

    Zhang, Yanli / Wang, Xiaocong / Hu, Cong / Yi, Huanfa

    Life Sciences. 2023 Mar., v. 316 p.121434-

    2023  

    Abstract: By interacting with DNA, RNA, and proteins, long noncoding RNAs (lncRNAs) have been linked to several pathological states. LncRNA-derived peptides, as a novel modality of action of lncRNAs, have recently become a research hotspot. An increasing body of ... ...

    Abstract By interacting with DNA, RNA, and proteins, long noncoding RNAs (lncRNAs) have been linked to several pathological states. LncRNA-derived peptides, as a novel modality of action of lncRNAs, have recently become a research hotspot. An increasing body of evidence has demonstrated the important role of these peptides in carcinogenesis and cancer progression and immune response. This review first describes lncRNA-derived peptides, the regulators that control their translation, and the roles of these peptides in multiple biological processes and disease states including cancers. In the following section, we comprehensively analyzed the significant role lncRNA-derived peptide played in the immune response. This review provides fresh perspectives on the biological role of lncRNAs and their relationship with diseases, particularly with cancers and the immune response, providing a theoretical basis for these lncRNA-derived peptides as therapeutic and diagnostic targets in cancers and inflammatory diseases.
    Keywords DNA ; RNA ; carcinogenesis ; immune response ; neoplasm progression ; peptides ; therapeutics ; transcription (genetics) ; Long noncoding RNA ; Inflammatory diseases ; Alternative splicing ; lncRNA ; ORF ; HCC ; CRC ; ESCC ; TNBC ; EVs ; PBMC ; BMDM
    Language English
    Dates of publication 2023-03
    Publishing place Elsevier Inc.
    Document type Article ; Online
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2023.121434
    Database NAL-Catalogue (AGRICOLA)

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  8. Article ; Online: Long Noncoding RNAs as Orchestrators of CD4+ T-Cell Fate

    Chang Liu / Yanli Zhang / Zhanchuan Ma / Huanfa Yi

    Frontiers in Cell and Developmental Biology, Vol

    2022  Volume 10

    Abstract: CD4+ T cells differentiate towards different subpopulations through the regulation of lineage-specific cytokines and transcription factors, which flexibly respond to various immune challenges. However, considerable work has demonstrated that the CD4+ T- ... ...

    Abstract CD4+ T cells differentiate towards different subpopulations through the regulation of lineage-specific cytokines and transcription factors, which flexibly respond to various immune challenges. However, considerable work has demonstrated that the CD4+ T-cell differentiation mechanism is complex and not limited to transcription factors and cytokines. Long noncoding RNAs (lncRNAs) are RNA molecules with lengths exceeding 200 base pairs that regulate various biological processes and genes. LncRNAs have been found to conciliate the plasticity of CD4+ T-cell differentiation. Then, we focused on lncRNAs involved in CD4+ T-cell differentiation and enlisted some molecular thought into the plasticity and functional heterogeneity of CD4+ T cells. Furthermore, elucidating how lncRNAs modulate CD4+ T-cell differentiation in disparate immune diseases may provide a basis for the pathological mechanism of immune-mediated diseases.
    Keywords long noncoding RNA ; plasticity ; CD4+ T-cell differentiation ; immune modulation ; immune diseases ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2022-06-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Oxidative stress as a culprit in diabetic kidney disease.

    Su, Sensen / Ma, Zhanchuan / Wu, Hao / Xu, Zhonggao / Yi, Huanfa

    Life sciences

    2023  Volume 322, Page(s) 121661

    Abstract: Diabetic kidney disease (DKD) has become the leading cause of end-stage renal disease (ESRD), and the prevalence of DKD has increased worldwide during recent years. DKD is associated with poor therapeutic outcomes in most patients, but there is limited ... ...

    Abstract Diabetic kidney disease (DKD) has become the leading cause of end-stage renal disease (ESRD), and the prevalence of DKD has increased worldwide during recent years. DKD is associated with poor therapeutic outcomes in most patients, but there is limited understanding of its pathogenesis. This review suggests that oxidative stress interacts with many other factors in causing DKD. Highly active mitochondria and NAD(P)H oxidase are major sources of oxidants, and they significantly affect the risk for DKD. Oxidative stress and inflammation may be considered reciprocal causes of DKD, in that each is a cause and an effect of DKD. Reactive oxygen species (ROS) can act as second messengers in various signaling pathways and as regulators of metabolism, activation, proliferation, differentiation, and apoptosis of immune cells. Epigenetic modifications, such as DNA methylation, histone modifications, and non-coding RNAs can modulate oxidative stress. The development of new technologies and identification of new epigenetic mechanisms may provide novel opportunities for the diagnosis and treatment of DKD. Clinical trials demonstrated that novel therapies which reduce oxidative stress can slow the progression of DKD. These therapies include the NRF2 activator bardoxolone methyl, new blood glucose-lowering drugs such as sodium-glucose cotransporter 2 inhibitors, and glucagon-like peptide-1 receptor agonists. Future studies should focus on improving early diagnosis and the development of more effective combination treatments for this multifactorial disease.
    MeSH term(s) Humans ; Diabetic Nephropathies/metabolism ; Kidney Failure, Chronic ; Oxidative Stress ; Epigenesis, Genetic ; Reactive Oxygen Species/metabolism ; Diabetes Mellitus/genetics
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2023-04-05
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2023.121661
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.368: Show issues Location:
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  10. Article ; Online: Regulation of DNA-PK activity promotes the progression of TNBC via enhancing the immunosuppressive function of myeloid-derived suppressor cells.

    Han, Jiawen / Wan, Minjie / Ma, Zhanchuan / Yi, Huanfa

    Cancer medicine

    2022  Volume 12, Issue 5, Page(s) 5939–5952

    Abstract: Background: DNA-dependent protein kinase (DNA-PK) is engaged in DNA damage repair and is significantly expressed in triple negative breast cancer (TNBC). Inhibiting DNA-PK to reduce DNA damage repair provides a possibility of tumor treatment. NU7441, a ... ...

    Abstract Background: DNA-dependent protein kinase (DNA-PK) is engaged in DNA damage repair and is significantly expressed in triple negative breast cancer (TNBC). Inhibiting DNA-PK to reduce DNA damage repair provides a possibility of tumor treatment. NU7441, a DNA-PK inhibitor, can regulate the function and differentiation of CD4
    Results: In this study, we found that NU7441 alone significantly increased tumor growth in 4 T1 (a mouse TNBC cell line) tumor-bearing mice. Bioinformatics analysis showed that DNA-PK and functional markers of MDSCs (iNOS, Arg1, and IDO) tended to coexist in breast cancer patients. The mutations of these genes were significantly correlated with lower survival in breast cancer patients. Moreover, NU7441 significantly decreased the percentage of MDSCs in peripheral blood mononuclear cells (PBMCs), spleen and tumor, but enhanced the immunosuppressive function of splenic MDSCs. Furthermore, NU7441 increased MDSCs' DNA-PK and pDNA-PK protein levels in PBMCs and in the spleen and increased DNA-PK mRNA expression and expression of MDSCs functional markers in splenic MDSCs from tumor-bearing mice. NU7441 combined with gemcitabine reduced tumor volume, which may be because gemcitabine eliminated the remaining MDSCs with enhanced immunosuppressive ability.
    Conclusions: These findings highlight that the regulation of DNA-PK activity by NU7441 promotes TNBC progression via enhancing the immunosuppressive function of MDSCs. Moreover, NU7441 combined with gemcitabine offers an efficient therapeutic approach for TNBC and merits deeper investigation.
    MeSH term(s) Animals ; Mice ; DNA/pharmacology ; Gemcitabine ; Leukocytes, Mononuclear ; Myeloid-Derived Suppressor Cells ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics
    Chemical Substances DNA (9007-49-2) ; Gemcitabine ; Prkdc protein, mouse (EC 2.7.11.1)
    Language English
    Publishing date 2022-11-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2659751-2
    ISSN 2045-7634 ; 2045-7634
    ISSN (online) 2045-7634
    ISSN 2045-7634
    DOI 10.1002/cam4.5387
    Database MEDical Literature Analysis and Retrieval System OnLINE

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