Elp3 activates the JNK/MAPK pathway through histone acetylation to promote gastric cancer proliferation, migration, and invasion.

IF 2 4区生物学 Q3 CELL BIOLOGY

Histology and histopathology Pub Date : 2025-10-06 DOI:10.14670/HH-25-001

Ji Di, Hao Shang, Xiali Shi, Hanmei Jiang

{"title":"Elp3 activates the JNK/MAPK pathway through histone acetylation to promote gastric cancer proliferation, migration, and invasion.","authors":"Ji Di, Hao Shang, Xiali Shi, Hanmei Jiang","doi":"10.14670/HH-25-001","DOIUrl":null,"url":null,"abstract":"Background: Gastric cancer (GC) seriously affects the life and health of patients, and the role of Elp3 in GC is still unclear; therefore, the aim of this study was to investigate the role and mechanism of Elp3 overexpression in GC.Methods: Elp3-overexpressing HGC27 cells were constructed with an overexpression plasmid, and Elp3-overexpressing GC nude mice were prepared, which were intervened by histone acetylation inhibitor (SAHA) or JNK pathway inhibitor (SP600125). The protein interactions between Elp3 and JNK1 were verified by Co-immunoprecipitation (Co-IP) assay. Cell proliferation, migration, invasion, JNK/MAPK pathway, and histopathological changes were evaluated with CCK-8, clone formation assay, scratch assay, Transwell, qRT-PCR, western blot, and HE staining.Results: Elp3 interacted with JNK1 protein, and Elp3 overexpression promoted GC proliferation, invasion, migration, elevated HAT activity, and activation of the JNK/MAPK pathway. A histone acetylation inhibitor attenuated the promotional effect of Elp3 overexpression on GC and activation of the JNK/MAPK pathway. Further, inhibition of the JNK/MAPK pathway also suppressed the promotion of GC by Elp3 overexpression.Conclusion: Elp3 may be involved in GC progression by activating the JNK/MAPK pathway through histone acetylation.","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25001"},"PeriodicalIF":2.0000,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Histology and histopathology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.14670/HH-25-001","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Gastric cancer (GC) seriously affects the life and health of patients, and the role of Elp3 in GC is still unclear; therefore, the aim of this study was to investigate the role and mechanism of Elp3 overexpression in GC.

Methods: Elp3-overexpressing HGC27 cells were constructed with an overexpression plasmid, and Elp3-overexpressing GC nude mice were prepared, which were intervened by histone acetylation inhibitor (SAHA) or JNK pathway inhibitor (SP600125). The protein interactions between Elp3 and JNK1 were verified by Co-immunoprecipitation (Co-IP) assay. Cell proliferation, migration, invasion, JNK/MAPK pathway, and histopathological changes were evaluated with CCK-8, clone formation assay, scratch assay, Transwell, qRT-PCR, western blot, and HE staining.

Results: Elp3 interacted with JNK1 protein, and Elp3 overexpression promoted GC proliferation, invasion, migration, elevated HAT activity, and activation of the JNK/MAPK pathway. A histone acetylation inhibitor attenuated the promotional effect of Elp3 overexpression on GC and activation of the JNK/MAPK pathway. Further, inhibition of the JNK/MAPK pathway also suppressed the promotion of GC by Elp3 overexpression.

Conclusion: Elp3 may be involved in GC progression by activating the JNK/MAPK pathway through histone acetylation.

查看原文本刊更多论文

Elp3通过组蛋白乙酰化激活JNK/MAPK通路，促进胃癌的增殖、迁移和侵袭。

背景：胃癌（胃癌）严重影响患者的生命和健康，Elp3在胃癌中的作用尚不清楚；因此，本研究旨在探讨Elp3过表达在胃癌中的作用和机制。方法：用过表达质粒构建elp3过表达的HGC27细胞，制备elp3过表达的GC裸鼠，用组蛋白乙酰化抑制剂（SAHA）或JNK通路抑制剂（SP600125）进行干预。通过共免疫沉淀（Co-IP）实验验证Elp3和JNK1之间的蛋白相互作用。采用CCK-8、克隆形成实验、划痕实验、Transwell、qRT-PCR、western blot、HE染色等方法评价细胞增殖、迁移、侵袭、JNK/MAPK通路及组织病理学变化。结果：Elp3与JNK1蛋白相互作用，Elp3过表达促进GC增殖、侵袭、迁移、HAT活性升高以及JNK/MAPK通路的激活。一种组蛋白乙酰化抑制剂减弱了Elp3过表达对GC的促进作用和JNK/MAPK通路的激活。此外，JNK/MAPK通路的抑制也抑制了Elp3过表达对GC的促进。结论：Elp3可能通过组蛋白乙酰化激活JNK/MAPK通路参与GC的进展。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Histology and histopathology 生物-病理学

CiteScore

3.90

自引率

0.00%

发文量

232

审稿时长

2 months

期刊介绍： HISTOLOGY AND HISTOPATHOLOGY is a peer-reviewed international journal, the purpose of which is to publish original and review articles in all fields of the microscopical morphology, cell biology and tissue engineering; high quality is the overall consideration. Its format is the standard international size of 21 x 27.7 cm. One volume is published every year (more than 1,300 pages, approximately 90 original works and 40 reviews). Each volume consists of 12 numbers published monthly online. The printed version of the journal includes 4 books every year; each of them compiles 3 numbers previously published online.