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Article ; Online: m

Wu, Xingwei / Fu, Minjie / Ge, Chang / Zhou, Hanyu / Huang, Haoyu / Zhong, Min / Zhang, Mengying / Xu, Hao / Zhu, Guoping / Hua, Wei / Lv, Kun / Yang, Hui

Molecular neurobiology

2024

Abstract: Long noncoding RNAs (lncRNAs) play crucial roles in tumor progression and are dysregulated in glioma. However, the functional roles of lncRNAs in glioma remain largely unknown. In this study, we utilized the TCGA (the Cancer Genome Atlas database) and ... ...

Abstract	Long noncoding RNAs (lncRNAs) play crucial roles in tumor progression and are dysregulated in glioma. However, the functional roles of lncRNAs in glioma remain largely unknown. In this study, we utilized the TCGA (the Cancer Genome Atlas database) and GEPIA2 (Gene Expression Profiling Interactive Analysis 2) databases and observed the overexpression of lncRNA CHASERR in glioma tissues. We subsequently investigated this phenomenon in glioma cell lines. The effects of lncRNA CHASERR on glioma proliferation, migration, and invasion were analyzed using in vitro and in vivo experiments. Additionally, the regulatory mechanisms among PTEN/p-Akt/mTOR and Wnt/β-catenin, lncRNA CHASERR, Micro-RNA-6893-3p(miR-6893-3p), and tripartite motif containing14 (TRIM14) were investigated via bioinformatics analyses, quantitative real-time PCR (qRT-PCR), western blot (WB), RNA immunoprecipitation (RIP), dual luciferase reporter assay, fluorescence in situ hybridization (FISH), and RNA sequencing assays. RIP and RT-qRCR were used to analyze the regulatory effect of N
Language	English
Publishing date	2024-01-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-023-03911-w
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 2411: Show issues

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Article ; Online: m

Wu, Jiamei / Yi, Tingzhuang / Zhuo, Chenyi / Wang, Duanduan / Zhang, Ming / Hu, Rui / Wu, Dan / Hou, Guoxin / Xing, Yutong

Journal of cellular physiology

2024

Abstract: Recent studies have indicated that dysregulation of the Hippo/Yes-associated protein (YAP) axis is associated with tumor progression and therapy resistance in various cancer types, including lung adenocarcinoma (LUAD). Understanding the regulation of ... ...

Abstract	Recent studies have indicated that dysregulation of the Hippo/Yes-associated protein (YAP) axis is associated with tumor progression and therapy resistance in various cancer types, including lung adenocarcinoma (LUAD). Understanding the regulation of Hippo signaling in LUAD is of great significance. Elevated levels of TRIB3, a pseudo kinase, have been observed in certain lung malignancies and are associated with an unfavorable prognosis. Our research aims to investigate whether increased TRIB3 levels enhance the malignant characteristics of LUAD cells and tumor progression through its interaction with the Hippo signaling pathway. In this study, we reported a positive correlation between elevated expression of TRIB3 and LUAD progression. Additionally, TRIB3 has the ability to enhance TEAD luciferase function and suppress Hippo pathway activity. Moreover, TRIB3 increases total YAP protein levels and promotes YAP nuclear localization. Mechanistic experiments revealed that TRIB3 directly interacts with large tumor suppressor kinase 1 (LATS1), thereby suppressing Hippo signaling. Moreover, the decrease in METTL3-mediated N6-methyladenosine modification of TRIB3 results in a substantial elevation of its expression levels in LUAD cells. Collectively, our research unveils a novel discovery that TRIB3 enhances the growth and invasion of LUAD cells by interacting with LATS1 and inhibiting the Hippo signaling pathway. TRIB3 may serve as a potential biomarker for an unfavorable prognosis and a target for novel treatments in YAP-driven lung cancer.
Language	English
Publishing date	2024-02-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.31220
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Uc I Zs.212: Show issues

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Article: M

Zhang, Xin / Sai, Linlin / Zhang, Weiliang / Kan, Xingzheng / Jia, Qiang / Bo, Cunxiang / Yin, Wenhui / Shao, Hua / Han, Mingming / Peng, Cheng

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

2023 Volume 45, Issue 1, Page(s) 23

Abstract: Background: Evidence showed that N: Results: The analysis showed that m: Conclusions ... These findings indicated that differentially m ...

Abstract	Background: Evidence showed that N Results: The analysis showed that m Conclusions: These findings indicated that differentially m
Language	English
Publishing date	2023-09-01
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/s41021-023-00279-0
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Article ; Online: m

Zhu, Xiaolong / Wu, Xingwei / Yang, Hui / Xu, Qiancheng / Zhang, Mengying / Liu, Xiaocen / Lv, Kun

Biology direct

2023 Volume 18, Issue 1, Page(s) 27

Abstract: ... methyladenine (m: Results: LINC01003 expression was upregulated in glioma cell lines and tissues. Higher ... LINC01003 upregulation is induced by m: Conclusion: This study characterized LINC01003 as a lncRNA ...

Abstract	Background: Long non-coding RNAs (lncRNAs) play important roles in the progression of glioma. Here, we examined the potential functions of a lncRNA, LINC01003, in glioma and characterized the underlying molecular mechanisms. Methods: The GEIPA2 and Chinese Glioma Genome Atlas (CCGA) databases were employed to analyze gene expression and the overall survival curve in patients with glioma. The functions of LINC01003 in glioma growth and migration were assessed by loss-of-function experiments in vitro and in vivo. RNA sequencing was used to determine the signaling pathways effected by LINC01003. Bioinformatics analysis and RNA immunoprecipitation (RIP) assays were used to explore the mechanism underlying the N6-methyladenine (m Results: LINC01003 expression was upregulated in glioma cell lines and tissues. Higher LINC01003 expression predicted shorter overall survival time in glioma patients. Functionally, LINC01003 knockdown inhibited the cell cycle and cell proliferation and migration in glioma cells. Mechanistically, RNA sequencing revealed that LINC01003 mediated the focal adhesion signaling pathway. Furthermore, LINC01003 upregulation is induced by m Conclusion: This study characterized LINC01003 as a lncRNA that contributes to tumorigenesis in glioma and demonstrated that the LINC01003-CAV1-FAK axis serves as a potential therapeutic target for glioma.
MeSH term(s)	Humans ; Up-Regulation ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Signal Transduction/genetics ; Glioma/genetics ; Glioma/metabolism ; Cell Movement/genetics ; Cell Proliferation/genetics ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; MicroRNAs/genetics ; Methyltransferases/genetics ; Methyltransferases/metabolism
Chemical Substances	RNA, Long Noncoding ; MicroRNAs ; METTL3 protein, human (EC 2.1.1.62) ; Methyltransferases (EC 2.1.1.-)
Language	English
Publishing date	2023-06-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2221028-3
ISSN	1745-6150 ; 1745-6150
ISSN (online)	1745-6150
ISSN	1745-6150
DOI	10.1186/s13062-023-00386-6
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Article ; Online: m

Wang, Xuefei / Chen, Chen / Sun, Hongwei / Mao, Kaiqiong / Yao, Jiameng / Zhang, Weiqiao / Zhan, Meixiao / Li, Hua-Bing / Zhang, Zhiren / Zhu, Shu / Lu, Ligong

Science China. Life sciences

2023 Volume 66, Issue 11, Page(s) 2543–2552

Abstract: ... ...

Abstract	N
MeSH term(s)	Animals ; Mice ; Th17 Cells ; Autoimmunity/genetics ; Encephalomyelitis, Autoimmune, Experimental/genetics ; Cell Differentiation/genetics ; Methyltransferases/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Mice, Inbred C57BL
Chemical Substances	Methyltransferases (EC 2.1.1.-) ; RNA, Messenger
Language	English
Publishing date	2023-06-29
Publishing country	China
Document type	Journal Article
ZDB-ID	2546732-3
ISSN	1869-1889 ; 1674-7305
ISSN (online)	1869-1889
ISSN	1674-7305
DOI	10.1007/s11427-022-2323-4
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Article ; Online: m

Cao, Xiaoxue / Geng, Qishun / Fan, Danping / Wang, Qiong / Wang, Xing / Zhang, Mengxiao / Zhao, Lu / Jiao, Yi / Deng, Tingting / Liu, Honglin / Zhou, Jing / Jia, Liqun / Xiao, Cheng

Molecular cancer

2023 Volume 22, Issue 1, Page(s) 42

Abstract: N6-methyladenosine (m ...

Abstract	N6-methyladenosine (m
MeSH term(s)	Humans ; Methylation ; Immune Evasion ; Tumor Microenvironment ; Adenosine ; Carcinogenesis
Chemical Substances	Adenosine (K72T3FS567)
Language	English
Publishing date	2023-03-01
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2091373-4
ISSN	1476-4598 ; 1476-4598
ISSN (online)	1476-4598
ISSN	1476-4598
DOI	10.1186/s12943-022-01704-8
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Article ; Online: m

Wang, Shiguan / Chen, Shanze / Sun, Jianfeng / Han, Pan / Xu, Bowen / Li, Xinying / Zhong, Youquan / Xu, Zaichao / Zhang, Peng / Mi, Ping / Zhang, Cuijuan / Li, Lixiang / Zhang, Haiyan / Xia, Yuchen / Li, Shiyang / Heikenwalder, Mathias / Yuan, Detian

Nature metabolism

2023 Volume 5, Issue 5, Page(s) 842–860

Abstract: ... adenosine (m ...

Abstract	Different organs undergo distinct transcriptional, epigenetic and physiological alterations that guarantee their functional maturation after birth. However, the roles of epitranscriptomic machineries in these processes have remained elusive. Here we demonstrate that expression of RNA methyltransferase enzymes Mettl3 and Mettl14 gradually declines during postnatal liver development in male mice. Liver-specific Mettl3 deficiency causes hepatocyte hypertrophy, liver injury and growth retardation. Transcriptomic and N6-methyl-adenosine (m
MeSH term(s)	Mice ; Male ; Animals ; Methyltransferases/genetics ; Methyltransferases/metabolism ; Liver/metabolism ; Hepatocytes/metabolism ; Ceramides ; Endoplasmic Reticulum Stress ; Adenosine/metabolism ; Sphingomyelin Phosphodiesterase/genetics ; Sphingomyelin Phosphodiesterase/metabolism
Chemical Substances	Methyltransferases (EC 2.1.1.-) ; Ceramides ; Adenosine (K72T3FS567) ; Smpd3 protein, mouse (EC 3.1.4.12) ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12)
Language	English
Publishing date	2023-05-15
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-023-00808-9
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Article ; Online: m

Chen, Li / Xia, Siwei / Wang, Feixia / Zhou, Yuanyuan / Wang, Shuqi / Yang, Ting / Li, Yang / Xu, Min / Zhou, Ya / Kong, Desong / Zhang, Zili / Shao, Jiangjuan / Xu, Xuefen / Zhang, Feng / Zheng, Shizhong

Pharmacological research

2023 Volume 189, Page(s) 106704

Abstract: The roles of nuclear receptor subfamily 1 group d member 1 (NR1D1) and the circadian clock in liver fibrosis remain unclear. Here, we showed that liver clock genes, especially NR1D1, were dysregulated in mice with carbon tetrachloride ( ... ...

Abstract	The roles of nuclear receptor subfamily 1 group d member 1 (NR1D1) and the circadian clock in liver fibrosis remain unclear. Here, we showed that liver clock genes, especially NR1D1, were dysregulated in mice with carbon tetrachloride (CCl
MeSH term(s)	Mice ; Animals ; Hepatic Stellate Cells ; Circadian Clocks ; Methylation ; Liver Cirrhosis/metabolism ; Liver ; Nucleotidyltransferases ; Carbon Tetrachloride/metabolism ; Carbon Tetrachloride/pharmacology ; Nuclear Receptor Subfamily 1, Group D, Member 1/metabolism
Chemical Substances	Nucleotidyltransferases (EC 2.7.7.-) ; Carbon Tetrachloride (CL2T97X0V0) ; Nr1d1 protein, mouse ; Nuclear Receptor Subfamily 1, Group D, Member 1
Language	English
Publishing date	2023-02-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2023.106704
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Zs.A 721: Show issues

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Article ; Online: M

Lu, Zexin / Xia, Wenjun / Huang, Yongqiang / Hou, Mingzheng / Chen, Hu / Zhou, Jiliu / Shan, Hongming / Zhang, Yi

IEEE transactions on medical imaging

2023 Volume 42, Issue 3, Page(s) 850–863

Abstract: Lowering the radiation dose in computed tomography (CT) can greatly reduce the potential risk to public health. However, the reconstructed images from dose-reduced CT or low-dose CT (LDCT) suffer from severe noise which compromises the subsequent ... ...

Abstract	Lowering the radiation dose in computed tomography (CT) can greatly reduce the potential risk to public health. However, the reconstructed images from dose-reduced CT or low-dose CT (LDCT) suffer from severe noise which compromises the subsequent diagnosis and analysis. Recently, convolutional neural networks have achieved promising results in removing noise from LDCT images. The network architectures that are used are either handcrafted or built on top of conventional networks such as ResNet and U-Net. Recent advances in neural network architecture search (NAS) have shown that the network architecture has a dramatic effect on the model performance. This indicates that current network architectures for LDCT may be suboptimal. Therefore, in this paper, we make the first attempt to apply NAS to LDCT and propose a multi-scale and multi-level memory-efficient NAS for LDCT denoising, termed M3NAS. On the one hand, the proposed M3NAS fuses features extracted by different scale cells to capture multi-scale image structural details. On the other hand, the proposed M3NAS can search a hybrid cell- and network-level structure for better performance. In addition, M3NAS can effectively reduce the number of model parameters and increase the speed of inference. Extensive experimental results on two different datasets demonstrate that the proposed M3NAS can achieve better performance and fewer parameters than several state-of-the-art methods. In addition, we also validate the effectiveness of the multi-scale and multi-level architecture for LDCT denoising, and present further analysis for different configurations of super-net.
MeSH term(s)	Signal-To-Noise Ratio ; Neural Networks, Computer ; Tomography, X-Ray Computed/methods
Chemical Substances	nas (64706-31-6)
Language	English
Publishing date	2023-03-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	622531-7
ISSN	1558-254X ; 0278-0062
ISSN (online)	1558-254X
ISSN	0278-0062
DOI	10.1109/TMI.2022.3219286
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Zs.A 2546: Show issues

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Article ; Online: m

Yu, Yi / Meng, Li-Li / Chen, Xiao-Yu / Fan, Hui-Ning / Chen, Ming / Zhang, Jing / Zhu, Jin-Shui

Cellular signalling

2023 Volume 108, Page(s) 110699

Abstract: Background: YTHDF3 as a N6-methyladenosine (m6A) reader participates in the development and progression of multiple cancer types, however, the prognosis, molecular biology and immune infiltration of YTHDF3 in gastric cancer (GC) have not been ... ...

Abstract	Background: YTHDF3 as a N6-methyladenosine (m6A) reader participates in the development and progression of multiple cancer types, however, the prognosis, molecular biology and immune infiltration of YTHDF3 in gastric cancer (GC) have not been investigated. Methods: The YTHDF3 expression profile and clinicopathological parameters of stomach adenocarcinoma (STAD) were downloaded from TCGA. The online websites and databases such as GEPIA2, cBioPortal, UALCAN, ImmuCellAl, xCell, TISIDB, GSCA were utilized for analysis of the association of YTHDF3 with STAD, including clinical prognosis, WGCNA and LASSO Cox regression analysis. Further functional assays such as RT-qPCR, Western blot, immunohistochemistry (IHC), immunofluorescence (IF), CCK-8, colony formation, EdU and Transwell assays were performed to determine the role of YTHDF3 in GC. Results: We found that YTHDF3 was upregulated in STAD tissue samples ascribed to its copy number amplification and associated with poor prognosis in patients with STAD. GO and KEGG analyses showed that YTHDF3-related differential genes were predominantly enriched in the proliferation, metabolism and immune signaling pathways. Knockdown of YTHDF3 repressed the growth and invasion of GC cells by inhibition of PI3K/AKT signaling. We then identified YTHDF3-related lncRNAs, miRNAs and mRNAs, and constructed their prognostic signatures in patients with STAD. Moreover, YTHDF3 associated with tumor immune infiltration such as CD8+ T cells, macrophages, Tregs, MHC molecules and chemokines, upregulated PD-L1 and CXCL1 and exerted a response to the immunotherapy in GC. Conclusions: YTHDF3 upregulation indicates poor prognosis and promotes GC cell growth and invasion by activating PI3K/AKT pathway and regulating immune microenvironment. The established YTHDF3-related signatures highlight the association of YTHDF3 with the clinical prognosis and immune cell infiltration in GC.
MeSH term(s)	Humans ; Adenocarcinoma ; Immunosuppression Therapy ; MicroRNAs ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt ; Stomach Neoplasms ; Tumor Microenvironment
Chemical Substances	MicroRNAs ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; YTHDF3 protein, human
Language	English
Publishing date	2023-05-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2023.110699
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Zs.A 2579: Show issues

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