Abnormal methylation mediated upregulation of LINC00857 boosts malignant progression of lung adenocarcinoma by modulating the miR-486-5p/NEK2 axis

IF 1.9 4区 医学 Q3 RESPIRATORY SYSTEM Clinical Respiratory Journal Pub Date : 2024-05-09 DOI:10.1111/crj.13765
Haoyu Fu, Mingming Zhang, Xiaohui Liu, Yiming Yang, Ying Xing
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Abstract

LINC00857 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.

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异常甲基化介导的 LINC00857 上调通过调节 miR-486-5p/NEK2 轴促进肺腺癌的恶性进展
LINC00857经常在各种癌症中表达失调,进而产生致癌作用;然而,其在启动子区的DNA甲基化状态以及肺腺癌(LUAD)进展的分子机制仍然鲜为人知。通过生物信息学分析,我们检测了 LINC00857 在 LUAD 中的表达状态和甲基化位点,并进一步研究了 LINC00857 作为竞争性内源性 RNA 在癌症进展中的特性。目前的研究发现,LINC00857在LUAD组织和细胞中的过表达主要是由启动子区的低甲基化引起的。敲除LINC00857能显著降低细胞增殖,阻碍细胞迁移和侵袭,抑制淋巴结转移,并增强放射敏感性。研究人员还在裸鼠模型中考察了 LINC00857 对肿瘤生长的影响。随后,还筛选了下游因子 miR-486-5p 和 NEK2,并研究了推定的调控轴。总之,甲基化介导的LINC00857过表达对miR-486-5p/NEK2轴的调控作用可能是LUAD进展的一种新机制。
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来源期刊
Clinical Respiratory Journal
Clinical Respiratory Journal 医学-呼吸系统
CiteScore
3.70
自引率
0.00%
发文量
104
审稿时长
>12 weeks
期刊介绍: Overview Effective with the 2016 volume, this journal will be published in an online-only format. Aims and Scope The Clinical Respiratory Journal (CRJ) provides a forum for clinical research in all areas of respiratory medicine from clinical lung disease to basic research relevant to the clinic. We publish original research, review articles, case studies, editorials and book reviews in all areas of clinical lung disease including: Asthma Allergy COPD Non-invasive ventilation Sleep related breathing disorders Interstitial lung diseases Lung cancer Clinical genetics Rhinitis Airway and lung infection Epidemiology Pediatrics CRJ provides a fast-track service for selected Phase II and Phase III trial studies. Keywords Clinical Respiratory Journal, respiratory, pulmonary, medicine, clinical, lung disease, Abstracting and Indexing Information Academic Search (EBSCO Publishing) Academic Search Alumni Edition (EBSCO Publishing) Embase (Elsevier) Health & Medical Collection (ProQuest) Health Research Premium Collection (ProQuest) HEED: Health Economic Evaluations Database (Wiley-Blackwell) Hospital Premium Collection (ProQuest) Journal Citation Reports/Science Edition (Clarivate Analytics) MEDLINE/PubMed (NLM) ProQuest Central (ProQuest) Science Citation Index Expanded (Clarivate Analytics) SCOPUS (Elsevier)
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