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Methionyl-tRNA synthetase 1 participates in hepatocellular carcinoma and its regulated gene profile possesses potent prognostic ability
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作者 Hai-Yan Bu Hong Huang +13 位作者 Jia Li Ze-Bing Huang Yan Huang Yu-Kun Huang Ai-Min Wang Li Wu Jiao Yuan Rong-Jun Wang Min Lu Song-Man Yu Pan-Pan Yi ya-yu chen Yu-Peng Jiang Xing-Wang Hu 《World Journal of Gastrointestinal Oncology》 2025年第9期299-324,共26页
BACKGROUND Hepatocellular carcinoma(HCC)is a significant global health challenge with rising incidence rates and poor prognoses.Aminoacyl-tRNA synthetases(ARSs)are important regulators implicated in the occurrence and... BACKGROUND Hepatocellular carcinoma(HCC)is a significant global health challenge with rising incidence rates and poor prognoses.Aminoacyl-tRNA synthetases(ARSs)are important regulators implicated in the occurrence and progression of several cancers.However,their specific function in HCC remains unclear,and ARSs-related prognostic factors for patient stratification are lacking.AIM To investigate the ARSs-related mechanisms of HCC and establish an effective prognostic risk model for stratifying patients with HCC.METHODS We screened ARSs genes of interest using differential gene expression,mutation,and survival analysis.Western blot and Immunohistochemistry were used to analyze MARS1 expression in the liver tissues of patients with HCC.Functional studies,including CCK-8 cell viability assay,EdU cell proliferation assay,cell cycle assays,Transwell migration and invasion assays,and in vivo tumor xenograft models,were conducted to comprehensively elucidate the specific role of MARS1 in HCC.Moreover,the MARS1-related prognostic score(MRPS)was established by LASSO regression and Cox regression analysis in The Cancer Genome Atlas-HCC and GSE14520 cohorts.Patients’immunotherapy and chemotherapy responses were predicted by immunomicroenvironment and drug susceptibility analysis in both subgroups.RESULTS MARS1 was selected as a target gene from a series of ARSs genes,with markedly higher expression observed in HCC tissues compared to adjacent non-cancerous tissues.Silencing MARS1 considerably impeded the proliferation,migration,invasion,and tumorigenic abilities of HCC cells in vitro and in vivo.Moreover,high MRPSs were associated with poor overall survival,altered infiltration of T cells,macrophages,monocytes,elevated immune checkpoint expression(PD-L1,CTLA4,LAG3),and reduced drug sensitivity in HCC.CONCLUSION MARS1 promotes HCC development and represents a potential therapeutic target for HCC management.Furthermore,MRPS serves as an independent prognostic factor for survival and a predictor of tumor treatment response. 展开更多
关键词 Methionyl-tRNA synthetase 1 Hepatocellular carcinoma Aminoacyl-tRNA synthetases Prognostic model BIOINFORMATICS
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Formation mechanism and growth kinetics of TiAl_(3) phase in cold-rolled Ti/Al laminated composites during annealing 被引量:7
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作者 Jian-yu ZHANG Yan-hui WANG +3 位作者 Zheng LÜ Qing-an chen ya-yu chen He-zong LI 《Transactions of Nonferrous Metals Society of China》 SCIE EI CAS CSCD 2022年第2期524-539,共16页
Cold-rolled Ti/Al laminated composites were annealed at 525−625℃for 0−128 h,and the interfacial microstructure evolution was investigated.The results indicate that only the TiAl_(3) phase was formed at the Ti/Al inte... Cold-rolled Ti/Al laminated composites were annealed at 525−625℃for 0−128 h,and the interfacial microstructure evolution was investigated.The results indicate that only the TiAl_(3) phase was formed at the Ti/Al interface;most of TiAl_(3) grains were fine equiaxed with average sizes ranging from hundreds of nanometers to several microns and the TiAl_(3) grain size increased with increasing annealing time and/or temperature,but the effect of annealing temperature on the TiAl_(3) grain size was far greater than that of annealing time.The growth of the TiAl_(3) phase consisted of two stages.The initial stage was governed by chemical reaction with a reaction activation energy of 195.75 kJ/mol,and the reaction rate constant of the TiAl_(3) phase was larger as the Ti/Al interface was bonded with fresh surfaces.At the second stage,the growth was governed by diffusion,the diffusion activation energy was 33.69 kJ/mol,and the diffusion growth rate constant of the TiAl_(3) phase was mainly determined by the grain boundary diffusion owing to the smaller TiAl_(3) grain size. 展开更多
关键词 Ti/Al laminated composites ANNEALING growth kinetics TiAl3 phase formation mechanism
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Anti-fibrotic effect of rosmarinic acid on inhibition of pterygium epithelial cells 被引量:4
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作者 ya-yu chen Chia-Fang Tsai +3 位作者 Ming-Chu Tsai Wen-Kang chen Yu-Wen Hsu Fung-Jou Lu 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2018年第2期189-195,共7页
AIM: To investigate the anti-fibrosis effect of rosmarinic acid(RA) in pterygium epithelial cells(PECs) to determine if RA is a potent agent for treating pterygium.METHODS: The PECs(1×10-4 cells/mL) were ... AIM: To investigate the anti-fibrosis effect of rosmarinic acid(RA) in pterygium epithelial cells(PECs) to determine if RA is a potent agent for treating pterygium.METHODS: The PECs(1×10-4 cells/mL) were treated with 100 μmol/L of RA for 1, 3 and 6h. After RA treatment, the cell viability was determined by staining with acridine orange/DAPI and analysis via a NucleoC ounter NC-3000. The protein expression levels of type I collagen, transforming growth factor beta-1(TGF-β1), TGF-β type Ⅱ receptor(TGF-βRⅡ), p-Smad1/5, p-Smad2, p-Smad3, and Smad4 of the cell lysates were measured by Western blot analysis.RESULTS: The cell viability of PECs was significantly decreased after RA treatment(P〈0.01). As the result, RA reduced the protein expression of typeⅠcollagen and TGF-β1 of PECs. Additionally, RA also inhibited TGF-β1/Smad signaling by decreasing the protein expressions of TGF-βRII, p-Smad1/5, p-Smad2, p-Smad3, and Smad4.CONCLUSION: This study demonstrate that RA could inhibit fibrosis of PECs by down-regulating type I collagen expression and TGF-β1/Smad signaling. Therefore, RA is a potent therapeutic agent for the treatment of pterygium. 展开更多
关键词 fibrosis pterygium rosmarinic acid transforming growth factor beta-1 typeⅠcollagen
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