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环境病理学,毒理学和肿瘤学期刊

每年出版 4 

ISSN 打印: 0731-8898

ISSN 在线: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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HDAC3-Mediated Repression of LncRNA-LET Regulates Gastric Cancer Cell Growth Proliferation, Invasion, Migration, and Apoptosis via MiR-548k

卷 40, 册 4, 2021, pp. 21-32
DOI: 10.1615/JEnvironPatholToxicolOncol.2021039050
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摘要

Emerging studies have indicated the aberrant expression of histone deacetylases (HDACs) is closely associated with the development of tumors. However, the regulatory roles of HDACs-regulated long noncoding RNAs (lncRNA) in gastric cancer (GC) remain largely unknown. In this study, the effects of HDAC3 and HDAC3-mediated lncRNA-LET on the progression of GC were investigated. The expressions of HDAC3, lncRNA-LET, and miR-548k in GC cell lines were analyzed. The biological functions of HDAC3 and lncRNA-LET were measured by CCK-8 assay, Transwell assay, Western blot analysis, and cell apoptosis assays. Chromatin immunoprecipitation and luciferase reporter assay verified the regulatory relationship between HDAC3 and lncRNA-LET, and lncRNA-LET and miR-548 in GC cells. HDAC3 was significantly overexpressed in GC cell lines compared to GES-1. Knockdown of HDAC3 suppressed the proliferation, invasion, and migration of AGS and SGC-7901 cells, while cell apoptosis was promoted. Silenced HDAC3 promoted histone acetylation in the promoter region of lncRNA-LET, subsequently upregulating the expression of lncRNA-LET in AGS and SGC-7901 cells. In addition, overexpressed lncRNA-LET notably inhibited the proliferation, invasion, and migration of GC cells, whereas apoptosis was enhanced. LncRNA-LET could function as the sponge of miR-548k. HDAC3 was able to regulate the progression of GC cells via the lncRNA-LET/miR-548k signaling pathway. We confirmed that the HDAC3/lncRNA-LET/miR-548k signal axis mediated the occurrence and development of GC, and HDAC3 could be a novel therapeutic target for the treatments of GC.

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