Xinyue Zhang, Xi Chen, Dongyuan Sun, Ning Song, Minmin Li, Wentian Zheng, Yang Yu, Gang Ding, Yingying Jiang
{"title":"ENAH-202通过调节ZNF502/VIM轴促进口腔鳞状细胞癌癌症的进展。","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":"{\"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}","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}
ENAH-202 promotes cancer progression in oral squamous cell carcinoma by regulating ZNF502/VIM axis
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.
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.
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