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Article: Correction: NCAPD2 is a favorable predictor of prognostic and immunotherapeutic biomarker for multiple cancer types including lung cancer.

Feng, Linyuan / Yang, Yang / Lin, Zhenhua / Cui, Minghua / Jin, Aihua / Cui, Aili

Genes and environment : the official journal of the Japanese Environmental Mutagen Society

2024 Volume 46, Issue 1, Page(s) 6

Language	English
Publishing date	2024-02-13
Publishing country	England
Document type	Published Erratum
ZDB-ID	2269162-5
ISSN	1880-7062 ; 1880-7046
ISSN (online)	1880-7062
ISSN	1880-7046
DOI	10.1186/s41021-024-00301-z
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Article: NCPAD2 is a favorable predictor of prognostic and immunotherapeutic biomarker for multiple cancer types including lung cancer.

Feng, Linyuan / Yang, Yang / Lin, Zhenhua / Cui, Minghua / Jin, Aihua / Cui, Aili

Genes and environment : the official journal of the Japanese Environmental Mutagen Society

2024 Volume 46, Issue 1, Page(s) 2

Abstract: Background: Non-SMC condensin I complex subunit D2 (NCAPD2) belongs to the chromosomal structural maintenance family. While the different contribution of NCAPD2 to chromosome in mitosis have been thoroughly investigated, much less is known about the ... ...

Abstract	Background: Non-SMC condensin I complex subunit D2 (NCAPD2) belongs to the chromosomal structural maintenance family. While the different contribution of NCAPD2 to chromosome in mitosis have been thoroughly investigated, much less is known about the expression of NCAPD2 in pan-cancer. Thus, we used a bioinformatics dataset to conduct a pan-cancer analysis of NCAPD2 to determine its regulatory role in tumors. Methods: Multiple online databases were analyzed NCAPD2 gene expression, protein level, patient survival and functional enrichment in pan-cancer. Genetic alteration and tumor stemness of NCAPD2 were analyzed using cBioPortal and SangerBox. The GSCA and CellMiner were used to explore the relationship between NCAPD2 and drug sensitivity. The diagnostic value of prognosis was evaluated by ROC curve. Subsequently, the immune infiltration level and immune subtype of NCAPD2 in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) were analyzed using TIMER1 and TISIDB. Results: NCAPD2 gene expression was significantly higher in most cancers and associated with clinical stage and poor prognosis. Genomic heterogeneity of NCAPD2 promoted the occurrence and development of tumors. GO enrichment analysis suggested NCAPD2 might be involved in DNA repair and immune response. NCAPD2 was involved in immune infiltration of LUAD and LUSC. ROC curves showed that NCAPD2 has important prognosis diagnostic value in LUAD and LUSC. Moreover, NCAPD2 was drug sensitive to topotecan, which may be an optimize immunotherapy. Conclusions: It was found that NCAPD2 was overexpressed in pan-cancers, which was associated with poor outcomes. Importantly, NCAPD2 could be a diagnostic marker and an immune related biomarker for LUAD and LUSC.
Language	English
Publishing date	2024-01-03
Publishing country	England
Document type	Journal Article
ZDB-ID	2269162-5
ISSN	1880-7062 ; 1880-7046
ISSN (online)	1880-7062
ISSN	1880-7046
DOI	10.1186/s41021-023-00291-4
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Article ; Online: An integrative pan-cancer analysis reveals the carcinogenic effects of NCAPH in human cancer.

Liu, Ying / Ma, Xiao / Feng, Linyuan / Lin, Zhenhua / Zhou, Xianchun

Mathematical biosciences and engineering : MBE

2022 Volume 20, Issue 1, Page(s) 76–92

Abstract: Background: Non-chromosomal structure maintenance protein condensin complex I subunit H (NCAPH) has been reported to play a regulatory role in a variety of cancers and is associated with tumor poor prognosis. This study aims to explore the potential ... ...

Abstract	Background: Non-chromosomal structure maintenance protein condensin complex I subunit H (NCAPH) has been reported to play a regulatory role in a variety of cancers and is associated with tumor poor prognosis. This study aims to explore the potential role of NCAPH with a view to providing insights on pathologic mechanisms. Methods: The expression of NCAPH in different tumors was explored by The Cancer Genome Atlas (TCGA) and Genotype Tissue Expression (GTEx). The prognostic value of NCAPH was retrieved through GEPIA and Kaplan-Meier Plotter databases. Tumor Immunity Estimation Resource (TIMER) and Single-Sample Gene Set Enrichment Analysis (GSEA) to search for the association of NCAPH with tumor immune infiltration. The cBioPortal and PhosphoSite Plus databases showed NCAPH phosphorylation status in tumors. Gene set enrichment analysis (GSEA) was performed using bioinformatics. Results: Our findings revealed that NCAPH showed high expression levels in a wide range of tumor types, and was strongly correlated with the prognosis of patients. Moreover, a higher phosphorylation level at S59, S67, S76, S190, S222 and T38 site was discovered in head and neck squamous cell carcinoma (HNSC). NCAPH overexpression was positively correlated with the infiltration level of CD8+T cells and myeloid dendritic infiltration in breast cancer and thymoma. Conclusions: The up-regulation of NCAPH was significantly correlated with the poor prognosis and immune infiltration in pan-cancer, and NCAPH could be served as a potential immunotherapeutic target for cancers.
MeSH term(s)	Humans ; CD8-Positive T-Lymphocytes ; Cell Cycle Proteins ; Computational Biology ; Databases, Factual ; Nuclear Proteins ; Neoplasms
Chemical Substances	Cell Cycle Proteins ; NCAPH protein, human ; Nuclear Proteins
Language	English
Publishing date	2022-09-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2265126-3
ISSN	1551-0018 ; 1551-0018
ISSN (online)	1551-0018
ISSN	1551-0018
DOI	10.3934/mbe.2023005
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Article ; Online: N-MYC-interacting protein enhances type II interferon signaling by inhibiting STAT1 sumoylation.

Feng, Linyuan / Li, Wanwei / Li, Xiaowen / Li, Xiaotian / Ran, Yanhong / Yang, Xiaoping / Deng, Zemin / Li, Hongjian

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 12, Page(s) e23281

Abstract: Signaling desensitization is key to limiting signal transduction duration and intensity. Signal transducer and activator of transcription 1 (STAT1) can mediate type II interferon (IFNγ)-induced immune responses, which are enhanced and inhibited by STAT1 ... ...

Abstract	Signaling desensitization is key to limiting signal transduction duration and intensity. Signal transducer and activator of transcription 1 (STAT1) can mediate type II interferon (IFNγ)-induced immune responses, which are enhanced and inhibited by STAT1 phosphorylation and sumoylation, respectively. Here, we identified an N-MYC interacting protein, NMI, which can enhance STAT1 phosphorylation and STAT1-mediated IFNγ immune responses by binding and sequestering the E2 SUMO conjugation enzyme, UBC9, and blocking STAT1 sumoylation. NMI facilitates UBC9 nucleus-to-cytoplasm translocation in response to IFNγ, thereby inhibiting STAT1 sumoylation. STAT1 phosphorylation at Y701 and sumoylation at K703 are mutually exclusive modifications that regulate IFNγ-dependent transcriptional responses. NMI could not alter the phosphorylation level of sumoylation-deficient STAT1 after IFNγ treatment. Thus, IFNγ signaling is modulated by NMI through sequestration of UBC9 in the cytoplasm, leading to inhibition of STAT1 sumoylation. Hence, NMI functions as a switch for STAT1 activation/inactivation cycles by modulating an IFNγ-induced desensitization mechanism.
MeSH term(s)	Interferon-gamma/metabolism ; Sumoylation ; Signal Transduction ; Phosphorylation ; STAT1 Transcription Factor/genetics
Chemical Substances	Interferon-gamma (82115-62-6) ; STAT1 Transcription Factor
Language	English
Publishing date	2023-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202301450RR
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The NQO1/p53/SREBP1 axis promotes hepatocellular carcinoma progression and metastasis by regulating Snail stability.

Wang, Xinyue / Liu, Ying / Han, Anna / Tang, Chunxiao / Xu, Ran / Feng, Linyuan / Yang, Yang / Chen, Liyan / Lin, Zhenhua

Oncogene

2022 Volume 41, Issue 47, Page(s) 5107–5120

Abstract: Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide, and its abnormal metabolism affects the survival and prognosis of patients. Recent studies have found that NAD(P)H quinone oxidoreductase-1 (NQO1) played an ...

Abstract	Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide, and its abnormal metabolism affects the survival and prognosis of patients. Recent studies have found that NAD(P)H quinone oxidoreductase-1 (NQO1) played an important role in tumor metabolism and malignant progression. However, the molecular mechanisms by which NQO1 regulates lipid metabolism during HCC progression remain unclear. In this study, bioinformatics analysis and immunohistochemical results showed that NQO1 was highly expressed in HCC tissues and its high expression was closely related to the poor prognosis of HCC patients. Overexpression of NQO1 promoted the cell proliferation, epithelial-to-mesenchymal transition (EMT) process, and angiogenesis of HCC cells. Luciferase reporter assay further revealed that NQO1/p53 could induce the transcriptional activity of SREBP1, consequently regulating HCC progression through lipid anabolism. In addition, Snail protein was stabilized by NQO1/p53/SREBP1 axis and triggered the EMT process, and participated in the regulatory role of NQO1/p53/SREBP1 axis in HCC. Together, these data indicated that NQO1/SREBP1 axis promoted the progression and metastasis of HCC, and might be a potential therapeutic target for HCC.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/pathology ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation/genetics ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic ; Liver Neoplasms/pathology ; NAD(P)H Dehydrogenase (Quinone)/genetics ; NAD(P)H Dehydrogenase (Quinone)/metabolism ; Neoplasm Metastasis ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	NAD(P)H Dehydrogenase (Quinone) (EC 1.6.5.2) ; NQO1 protein, human (EC 1.6.5.2) ; Tumor Suppressor Protein p53 ; SREBF1 protein, human
Language	English
Publishing date	2022-10-17
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/s41388-022-02477-6
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Zs.A 2218: Show issues

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Article ; Online: NSP6 inhibits the production of ACE2-containing exosomes to promote SARS-CoV-2 infectivity.

Lv, Xi / Chen, Ran / Liang, Taizhen / Peng, Haojie / Fang, Qiannan / Xiao, Shiqi / Liu, Sen / Hu, Meilin / Yu, Fei / Cao, Lixue / Zhang, Yiwen / Pan, Ting / Xi, Zhihui / Ding, Yao / Feng, Linyuan / Zeng, Tao / Huang, Wenjing / Zhang, Hui / Ma, Xiancai

mBio

2024 Volume 15, Issue 3, Page(s) e0335823

Abstract: The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has triggered a global pandemic, which severely endangers public health. Our and others' works have shown that the angiotensin-converting enzyme 2 (ACE2)-containing exosomes ( ... ...

Abstract	The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has triggered a global pandemic, which severely endangers public health. Our and others' works have shown that the angiotensin-converting enzyme 2 (ACE2)-containing exosomes (ACE2-exos) have superior antiviral efficacies, especially in response to emerging variants. However, the mechanisms of how the virus counteracts the host and regulates ACE2-exos remain unclear. Here, we identified that SARS-CoV-2 nonstructural protein 6 (NSP6) inhibits the production of ACE2-exos by affecting the protein level of ACE2 as well as tetraspanin-CD63 which is a key factor for exosome biogenesis. We further found that the protein stability of CD63 and ACE2 is maintained by the deubiquitination of proteasome 26S subunit, non-ATPase 12 (PSMD12). NSP6 interacts with PSMD12 and counteracts its function, consequently promoting the degradation of CD63 and ACE2. As a result, NSP6 diminishes the antiviral efficacy of ACE2-exos and facilitates the virus to infect healthy bystander cells. Overall, our study provides a valuable target for the discovery of promising drugs for the treatment of coronavirus disease 2019. Importance: The outbreak of coronavirus disease 2019 (COVID-19) severely endangers global public health. The efficacy of vaccines and antibodies declined with the rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mutants. Angiotensin-converting enzyme 2-containing exosomes (ACE2-exos) therapy exhibits a broad neutralizing activity, which could be used against various viral mutations. Our study here revealed that SARS-CoV-2 nonstructural protein 6 inhibited the production of ACE2-exos, thereby promoting viral infection to the adjacent bystander cells. The identification of a new target for blocking SARS-CoV-2 depends on fully understanding the virus-host interaction networks. Our study sheds light on the mechanism by which the virus resists the host exosome defenses, which would facilitate the study and design of ACE2-exos-based therapeutics for COVID-19.
MeSH term(s)	Humans ; COVID-19/metabolism ; SARS-CoV-2/metabolism ; Angiotensin-Converting Enzyme 2/metabolism ; Exosomes/metabolism ; Peptidyl-Dipeptidase A/metabolism ; Antiviral Agents/pharmacology ; Spike Glycoprotein, Coronavirus/metabolism ; Protein Binding
Chemical Substances	Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Antiviral Agents ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
Language	English
Publishing date	2024-02-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.03358-23
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Article ; Online: Downregulation of N-myc Interactor Promotes Cervical Cancer Cells Growth by Activating Stat3 Signaling.

Wu, Songbin / Li, Xiaotian / Chai, Huizi / Feng, Linyuan / Li, Wenjing / Li, Hongjian

Cell biochemistry and biophysics

2020 Volume 79, Issue 1, Page(s) 103–111

Abstract: N-myc interactor (NMI), a member of the oncogene Myc family, has been reported to be closely related to the development of cancer. However, the character of NMI in cervical carcinoma has not been reported. Herein, we found that downregulation of NMI ... ...

Abstract	N-myc interactor (NMI), a member of the oncogene Myc family, has been reported to be closely related to the development of cancer. However, the character of NMI in cervical carcinoma has not been reported. Herein, we found that downregulation of NMI protein not only promoted the proliferation, migration, and invasion of HeLa cells, but also decreased their expression of Caspase-3 and Caspase-9. Silencing NMI promotes the epithelial-mesenchymal transition of human cervical carcinoma HeLa cells by upregulating N-cadherin, vimentin, and downregulating E-cadherin. Further investigation illustrated the downregulation of NMI can activate the STAT3 signaling pathway. In conclusion, we found that the downregulation of NMI plays an important role in the progression of cervical cancer, and may served as a novel therapeutic target for cervical cancer.
MeSH term(s)	Caspase 3/biosynthesis ; Caspase 9/biosynthesis ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Down-Regulation ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; HEK293 Cells ; HeLa Cells ; Humans ; N-Myc Proto-Oncogene Protein/biosynthesis ; Neoplasm Invasiveness ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Uterine Cervical Neoplasms/metabolism
Chemical Substances	MYCN protein, human ; N-Myc Proto-Oncogene Protein ; STAT3 Transcription Factor ; STAT3 protein, human ; CASP3 protein, human (EC 3.4.22.-) ; CASP9 protein, human (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Caspase 9 (EC 3.4.22.-)
Language	English
Publishing date	2020-10-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	1357904-6
ISSN	1559-0283 ; 1085-9195
ISSN (online)	1559-0283
ISSN	1085-9195
DOI	10.1007/s12013-020-00943-0
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Zs.A 1498: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Generation and Application of Mouse Monoclonal Antibody Against Human Cytomegalovirus UL23.

Li, Wenjing / Chai, Huizi / Feng, Linyuan / Deng, Jinfeng / Yang, Xiaoping / Ran, Yanhong / Li, Hongjian

Viral immunology

2020 Volume 33, Issue 5, Page(s) 378–383

Abstract: Human cytomegalovirus (HCMV) is a paradigm for pathogen-mediated immune evasion. The immune response to HCMV has been intensively studied for many years and still remains the focus of attention for numerous research groups. ...

Abstract	Human cytomegalovirus (HCMV) is a paradigm for pathogen-mediated immune evasion. The immune response to HCMV has been intensively studied for many years and still remains the focus of attention for numerous research groups.
MeSH term(s)	Animals ; Antibodies, Monoclonal/biosynthesis ; Antibodies, Monoclonal/immunology ; Antigens, Viral/genetics ; Antigens, Viral/immunology ; Cytomegalovirus/immunology ; Female ; Fibroblasts/immunology ; Fibroblasts/virology ; Fluorescent Antibody Technique, Direct ; Foreskin/cytology ; HEK293 Cells ; Humans ; Hybridomas/immunology ; Immediate-Early Proteins/genetics ; Immediate-Early Proteins/immunology ; Immunoglobulin G/biosynthesis ; Immunoglobulin G/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Recombinant Proteins/biosynthesis ; Recombinant Proteins/immunology
Chemical Substances	Antibodies, Monoclonal ; Antigens, Viral ; Immediate-Early Proteins ; Immunoglobulin G ; Recombinant Proteins ; immediate-early proteins, cytomegalovirus
Language	English
Publishing date	2020-03-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639075-4
ISSN	1557-8976 ; 0882-8245
ISSN (online)	1557-8976
ISSN	0882-8245
DOI	10.1089/vim.2019.0180
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Zs.A 2227: Show issues

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Article: Human Cytomegalovirus UL23 Attenuates Signal Transducer and Activator of Transcription 1 Phosphorylation and Type I Interferon Response.

Feng, Linyuan / Li, Wanwei / Wu, Xingyuan / Li, Xiaotian / Yang, Xiaoping / Ran, Yanhong / Wu, Jianguo / Li, Hongjian

Frontiers in microbiology

2021 Volume 12, Page(s) 692515

Abstract: Human cytomegalovirus (HCMV), the human beta-herpesvirus, can cause severe syndromes among both immunocompromised adult patients and newborns. Type I interferon (IFN-I) exerts an important effect to resist infections caused by viruses such as HCMV, while ...

Abstract	Human cytomegalovirus (HCMV), the human beta-herpesvirus, can cause severe syndromes among both immunocompromised adult patients and newborns. Type I interferon (IFN-I) exerts an important effect to resist infections caused by viruses such as HCMV, while IFN evasion may serve as a key determining factor for viral dissemination and disease occurrence within hosts. In this study, UL23, a tegument protein of HCMV, was confirmed to be a key factor for negatively regulating the type I IFN immune response. A detailed analysis indicated that the viral UL23 protein increases the IFN-I antiviral resistance during HCMV infections. Furthermore, UL23 was shown to significantly reduce the levels of IFN-stimulated genes (ISGs) and promoter activity of IFN-I-stimulated response element. Mechanically, UL23 was discovered to impair the signal transducer and activator of transcription 1 (STAT1) phosphorylation, although it was not found to affect phosphorylation and expression of STAT2, Janus activated kinase 1, or tyrosine kinase 2, which are associated with IFN-I signal transduction pathway. Additionally, a significantly reduced nuclear expression of STAT1 but not of IFN regulatory factor 9 or STAT2 was observed. Findings of this study indicate that HCMV UL23 is a viral antagonist that acts against the cellular innate immunity and reveal a possible novel effect of UL23 on IFN-I signaling.
Language	English
Publishing date	2021-07-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587354-4
ISSN	1664-302X
ISSN	1664-302X
DOI	10.3389/fmicb.2021.692515
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Article ; Online: Preparation and identification of polyclonal antibody against human cytomegalovirus encoding protein UL23.

Chai, Huizi / Wu, Songbin / Deng, Jinfeng / Feng, Linyuan / Yang, Xiaoping / Ran, Yanhong / Li, Hongjian

Protein expression and purification

2019 Volume 161, Page(s) 78–83

Abstract: Human cytomegalovirus (HCMV), a member of the human herpesvirus family, is a common opportunistic virus causing severe ailments and deaths in people with immature or compromised immune systems. UL23 is a virion protein found in the tegument and is ... ...

Abstract	Human cytomegalovirus (HCMV), a member of the human herpesvirus family, is a common opportunistic virus causing severe ailments and deaths in people with immature or compromised immune systems. UL23 is a virion protein found in the tegument and is expressed in the cytoplasm in HCMV infected cells. However, UL23 is dispensable for viral replication in cultured cells and little is currently known about its function. In order to further study of UL23, polyclonal antibody of UL23 was prepared. UL23 gene fragment was cloned from HCMV Towne by PCR and ligated into pET28a (+). The recombinant plasmid pET28a (+)-UL23 was transformed into E.coli BL21(DE3) to induce expression of the target protein. Then we efficiently purified the recombinant protein affinity chromatography under unique denaturation conditions. Recombinant UL23 protein was used as immunogen to inoculate New Zealand white rabbits and the sera was collected after the fourth immunization. UL23 Polyclonal antibody was purified from antisera using CNBr-activated Sepharose 4 beads. Our UL23 Polyclonal antibody showed specific reaction with UL23 in ELISA, Western-blot and immunofluorescence. More importantly, UL23 Polyclonal antibody could specifically recognize UL23 protein in HCMV infected cells, which laid a foundation for further study of HCMV UL23.
MeSH term(s)	Animals ; Antibodies/analysis ; Antibodies/immunology ; Antibodies/isolation & purification ; Cytomegalovirus/genetics ; Cytomegalovirus/metabolism ; Cytomegalovirus Infections/virology ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Gene Expression ; Humans ; Immunization ; Rabbits ; Recombinant Proteins/analysis ; Recombinant Proteins/genetics ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/metabolism ; Viral Proteins/analysis ; Viral Proteins/genetics ; Viral Proteins/isolation & purification ; Viral Proteins/metabolism
Chemical Substances	Antibodies ; Recombinant Proteins ; Viral Proteins
Language	English
Publishing date	2019-05-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1055455-5
ISSN	1096-0279 ; 1046-5928
ISSN (online)	1096-0279
ISSN	1046-5928
DOI	10.1016/j.pep.2019.04.008
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