ENAH-202 promotes cancer progression in oral squamous cell carcinoma by regulating ZNF502/VIM axis

IF 2.9 2区医学 Q2 ONCOLOGY Cancer Medicine Pub Date : 2023-10-30 DOI:10.1002/cam4.6652

Xinyue Zhang, Xi Chen, Dongyuan Sun, Ning Song, Minmin Li, Wentian Zheng, Yang Yu, Gang Ding, Yingying Jiang

{"title":"ENAH-202 promotes cancer progression in oral squamous cell carcinoma by regulating ZNF502/VIM axis","authors":"Xinyue Zhang, Xi Chen, Dongyuan Sun, Ning Song, Minmin Li, Wentian Zheng, Yang Yu, Gang Ding, Yingying Jiang","doi":"10.1002/cam4.6652","DOIUrl":null,"url":null,"abstract":"Abstract Background We aimed to demonstrate the regulatory effect of long non‐coding RNA (lncRNA) ENAH‐202 on oral squamous cell carcinoma (OSCC) development as well as its molecular mechanism. Methods We detected ENAH‐202 expression in OSCC tissues and cell lines by quantitative real‐time PCR (qPCR). The biological function of ENAH‐202 was assessed in vitro and in vivo using CCK‐8, colony formation assays, transwell assays, xenograft formation, and tail vein injection. The further molecular mechanism by which ENAH‐202 promoted OSCC progression was identified using RNA pull‐down, LS‐MS/MS analysis, RNA immunoprecipitation (RIP), and chromatin immunoprecipitation (ChIP) assays. Results ENAH‐202 was significantly upregulated in OSCC tissues and cells. ENAH‐202 promoted OSCC cell proliferation, migration, and invasion in vitro and in vivo. The expression of enabled homolog (ENAH) and epithelial‐to‐mesenchymal transition (EMT)‐related proteins was changed with the expression of ENAH‐202. Moreover, ENAH‐202 promoted the transcription of Vimentin (VIM) by binding with ZNF502, which can help ENAH‐202 promote OSCC progression. Conclusions ENAH‐202 facilitated OSCC cell proliferation and metastasis by regulating ZNF502/VIM axis, which played an important role in OSCC progression.","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"12 22","pages":"20892-20905"},"PeriodicalIF":2.9000,"publicationDate":"2023-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.6652","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Medicine","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cam4.6652","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Abstract Background We aimed to demonstrate the regulatory effect of long non‐coding RNA (lncRNA) ENAH‐202 on oral squamous cell carcinoma (OSCC) development as well as its molecular mechanism. Methods We detected ENAH‐202 expression in OSCC tissues and cell lines by quantitative real‐time PCR (qPCR). The biological function of ENAH‐202 was assessed in vitro and in vivo using CCK‐8, colony formation assays, transwell assays, xenograft formation, and tail vein injection. The further molecular mechanism by which ENAH‐202 promoted OSCC progression was identified using RNA pull‐down, LS‐MS/MS analysis, RNA immunoprecipitation (RIP), and chromatin immunoprecipitation (ChIP) assays. Results ENAH‐202 was significantly upregulated in OSCC tissues and cells. ENAH‐202 promoted OSCC cell proliferation, migration, and invasion in vitro and in vivo. The expression of enabled homolog (ENAH) and epithelial‐to‐mesenchymal transition (EMT)‐related proteins was changed with the expression of ENAH‐202. Moreover, ENAH‐202 promoted the transcription of Vimentin (VIM) by binding with ZNF502, which can help ENAH‐202 promote OSCC progression. Conclusions ENAH‐202 facilitated OSCC cell proliferation and metastasis by regulating ZNF502/VIM axis, which played an important role in OSCC progression.

Abstract Image

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

ENAH-202通过调节ZNF502/VIM轴促进口腔鳞状细胞癌癌症的进展。

背景：我们旨在证明长非编码RNA（lncRNA）ENAH-202对口腔鳞状细胞癌（OSCC）发展的调节作用及其分子机制。方法：采用实时定量PCR（qPCR）方法检测ENAH-202在口腔鳞癌组织和细胞系中的表达。使用CCK-8、集落形成测定、transwell测定、异种移植物形成和尾静脉注射在体外和体内评估ENAH-202的生物学功能。使用RNA下拉、LS-MS/MS分析、RNA免疫沉淀（RIP）和染色质免疫沉淀（ChIP）分析确定了ENAH-202促进OSCC进展的进一步分子机制。结果：ENAH-202在OSCC组织和细胞中表达显著上调。ENAH-202在体外和体内均能促进OSCC细胞的增殖、迁移和侵袭。使能同源物（ENAH）和上皮-间质转化（EMT）相关蛋白的表达随着ENAH-202的表达而改变。此外，ENAH-202通过与ZNF502结合促进波形蛋白（VIM）的转录，这可以帮助ENAH-202促进OSCC的进展。结论：ENAH-202通过调节ZNF502/VIM轴促进OSCC细胞的增殖和转移，在OSCC的进展中起重要作用。

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分钟内获得全文去求助

来源期刊

Cancer Medicine ONCOLOGY-

CiteScore

5.50

自引率

2.50%

发文量

907

审稿时长

19 weeks

期刊介绍： Cancer Medicine is a peer-reviewed, open access, interdisciplinary journal providing rapid publication of research from global biomedical researchers across the cancer sciences. The journal will consider submissions from all oncologic specialties, including, but not limited to, the following areas: Clinical Cancer Research Translational research ∙ clinical trials ∙ chemotherapy ∙ radiation therapy ∙ surgical therapy ∙ clinical observations ∙ clinical guidelines ∙ genetic consultation ∙ ethical considerations Cancer Biology: Molecular biology ∙ cellular biology ∙ molecular genetics ∙ genomics ∙ immunology ∙ epigenetics ∙ metabolic studies ∙ proteomics ∙ cytopathology ∙ carcinogenesis ∙ drug discovery and delivery. Cancer Prevention: Behavioral science ∙ psychosocial studies ∙ screening ∙ nutrition ∙ epidemiology and prevention ∙ community outreach. Bioinformatics: Gene expressions profiles ∙ gene regulation networks ∙ genome bioinformatics ∙ pathwayanalysis ∙ prognostic biomarkers. Cancer Medicine publishes original research articles, systematic reviews, meta-analyses, and research methods papers, along with invited editorials and commentaries. Original research papers must report well-conducted research with conclusions supported by the data presented in the paper.