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Using bioinformatics, the study analyzed LINC00857 expression and methylation in LUAD and tested its role as a competitive endogenous RNA. Results show promoter hypomethylation drives LINC00857 overexpression, while its knockdown reduces proliferation, migration, invasion, lymph node metastasis, and enhances radiosensitivity. Downstream miR-486-5p and NEK2 were identified, supporting a methylation-mediated LINC00857–miR-486-5p/NEK2 regulatory axis.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/abnormal-methylation-mediated-upregulation-of-linc00857-boosts-malignant-progression-of-lung-adenocarcinoma-by-modulating-the-mir-486-5pnek2-axis/332053/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/abnormal-methylation-mediated-upregulation-of-linc00857-boosts-malignant-progression-of-lung-adenocarcinoma-by-modulating-the-mir-486-5pnek2-axis/332053.png","ImageObject",300,407,{"name":92,"@type":93},"Aurora","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-23","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":39},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What mechanism links LINC00857 overexpression to LUAD progression?","Question",{"text":112,"@type":113},"LINC00857 overexpression in LUAD is mainly driven by hypomethylation of its promoter region, which then activates downstream effects on cancer phenotypes.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"What experimental effects does LINC00857 knockdown produce in LUAD cells?",{"text":117,"@type":113},"LINC00857 knockdown reduces cell proliferation, impedes migration and invasion, restrains lymph node metastasis, and enhances radiosensitivity.",{"name":119,"@type":110,"acceptedAnswer":120},"Which downstream axis is implicated by the study?",{"text":121,"@type":113},"The study screens and examines downstream factors miR-486-5p and NEK2, proposing a methylation-mediated regulatory axis: LINC00857–miR-486-5p/NEK2.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},332053,1790195727,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":39,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145,"preview_page_count":4},4810365810221,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","DOI: 10.1111/crj.13765  \nORIGINAL ARTICL E  \nAbnormal methylation mediated upregulation of LINC00857 boosts malignant progression of lung adenocarcinoma by modulating the miR-486-5p/NEK2 axis  \nHaoyu Fu 1  | Mingming Zhang 2 | Xiaohui Liu 2 | Yiming Yang 3 | Ying Xing 1  \n1Department of Radiation Oncology, Tangshan People’s Hospital, Tangshan, China  \n2Department of Thoracic Surgery, Tangshan People’s Hospital, Tangshan, China  \n3Department of Breast Surgery, Tangshan People’s Hospital, Tangshan, China  \nCorrespondence  \nHaoyu Fu, Department of Radiation Oncology, Tangshan People’s Hospital, No.65 Shengli Road, Lunan District, Tangshan, Hebei 063001, China.  \nEmail: [fhy063001@163.com](fhy063001@163.com)  \nFunding information  \nKey Project Program of Medical Science Research in Hebei Province, Grant/Award Number: 20171286  \n1 | INTRODUCTION  \nAbstract  \nLINC00857 is frequently dysregulated in varying cancers, which in turn exerts carcinogenic effects; however, its DNA methylation status in promoter region and molecular mechanisms underlying the progression of lung adenocarcinoma (LUAD) remain rarely understood. Through bioinformatics analysis, we examined the expression state and methylation site of LINC00857 in LUAD and further investigated the properties of LINC00857 as a competitive endogenous RNA in the cancer progression. The current study revealed that the overexpression of LINC00857 in LUAD tissue and cells was mainly caused by the hypomethylation of the promoter region. LINC00857 knockdown prominently reduced cell proliferation, impeded cell migration and invasion, and restrained lymph node metastasis, with enhancing radiosensitivity. The effects of LINC00857 on tumor growth were also investigated in nude mice models. Subsequently, the downstream factors, miR-486-5p and NEK2, were screened, and the putative regulatory axis was examined. Overall, the regulatory effect of methylation-mediated LINC00857 overexpression on miR-486-5p/NEK2 axis may be a new mechanism for LUAD progression.  \nKEYWORDS  \nLINC00857, LUAD, metastasis, methylation, radiosensitivity  \ncascade in those patients.4 Hence, elucidating mechanism underlying the LUAD occurrence and metastasis is criti-  \nEach year, at least one million deaths are caused by lung cancer, which is mostly responsible for deathrate associated with cancer globally. Lung adenocarcinoma (LUAD) is a prevalent histology.1 LUAD is found almost exclusively in peripheral lung tissue and arises from smaller airways.2 Surgery is suggested for patients with early LUAD, but most patients are suffering from an early relapse, in the first 2 years, after complete resection,3 which could be attributed to metastatic  \ncal to provide better treatment strategies for LUAD.  \nEpigenetics is a major promising area within current biomedical fields.5 As a critical mechanism of epigenesis, DNA methylation is key in regulating gene expression, chromatin modification, genome imprinting, and stabilization.6 Abnormal DNA methylation is increasingly being associated with the pathogenesis of many human cancers.6 For example, in lung cancer, ADAMTS18 was hindered by promoter CpG methylation and enhanced  \nThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.  \n© 2024 The Authors. The Clinical Respiratory Journal published by John Wiley & Sons Ltd.  \nClin Respir J. 2024;18:e13765 .  \n[https://doi.org/10.1111/crj.13765](https://doi.org/10.1111/crj.13765)  \n[wileyonlinelibrary.com/journal/crj](wileyonlinelibrary.com/journal/crj)  \n1 of 14  \ncisplatin sensitivity through EGFR/AKT signaling.7 Hypomethylation-induced upregulation of cancer/testis antigen KK-LC-1 promoted the LUAD development via activation of Notch1/Hes1 signaling.8 DNA methylation pattern of cancer cells impacts levels of protein-coding genes and tumor-related lncRNAs. Zhi et al. reported a computatio","cbCaia7Py90tWP7N","https://ap.wps.com/l/cbCaia7Py90tWP7N","pdf",4012604,14,"English","# INTRODUCTION\n## Background: LUAD burden and relapse\n## Epigenetics and DNA methylation in cancer\n## ceRNA regulation by lncRNAs\n## Prior evidence linking LINC00857 to cancers","[{\"question\":\"What mechanism links LINC00857 overexpression to LUAD progression?\",\"answer\":\"LINC00857 overexpression in LUAD is mainly driven by hypomethylation of its promoter region, which then activates downstream effects on cancer phenotypes.\"},{\"question\":\"What experimental effects does LINC00857 knockdown produce in LUAD cells?\",\"answer\":\"LINC00857 knockdown reduces cell proliferation, impedes migration and invasion, restrains lymph node metastasis, and enhances radiosensitivity.\"},{\"question\":\"Which downstream axis is implicated by the study?\",\"answer\":\"The study screens and examines downstream factors miR-486-5p and NEK2, proposing a methylation-mediated regulatory axis: LINC00857–miR-486-5p/NEK2.\"}]","Abnormal methylation mediated upregulation of LINC00857 boosts malignant progression of lung adenocarcinoma by modulating the miR-486-5p/NEK2 axis | PDF",1789996500,35]