竞争性内源性RNA
腺癌
癌症研究
生物
肺癌
抑制器
肿瘤微环境
小RNA
基因
转录组
癌症
基因表达
下调和上调
肿瘤科
肿瘤细胞
遗传学
医学
长非编码RNA
作者
Defang Ding,Jingyu Zhong,Yue Xing,Yangfan Hu,Xiang Ge,Weiwu Yao
出处
期刊:Current Cancer Drug Targets
[Bentham Science]
日期:2023-11-30
卷期号:24 (6): 654-667
标识
DOI:10.2174/0115680096266700231107071222
摘要
Background:: Lung adenocarcinoma (LUAD) is a major health challenge worldwide with an undesirable prognosis. LINC00982 has been implicated as a tumor suppressor in diverse human cancers; however, its role in LUAD has not been fully characterized. Methods:: Expression level and prognostic value of LINC00982 were investigated in pan-cancer and lung cancer from The Cancer Genome Atlas (TCGA) project. Differential expression analysis based on the LINC00982 expression level was performed in LUAD followed by gene set enrichment analysis (GSEA) and functional enrichment analyses. The association between LINC00982 expression and tumor immune microenvironment characteristics was evaluated. A potential ceRNA regulatory axis was identified and experimentally validated. Results:: We found that LINC00982 expression was downregulated and correlated with poor prognosis in LUAD. Enrichment analyses revealed that LINC00982 could inhibit DNA damage repair and cell proliferation, but enhance tumor metabolic reprogramming. We identified a competing endogenous RNA network involving LINC00982, miR-183-5p, and ATP-binding cassette subfamily A member 8 (ABCA8). Luciferase assays confirmed that miR-183-5p can interact with LINC00982 and ABCA8. Forced miR-183-5p expression reduced LINC00982 transcript levels and suppressed ABCA8 expression. Conclusions:: Our findings revealed the LINC00982/miR-183-5p/ABCA8 axis as a potential therapeutic target in LUAD.
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