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检测与透明细胞肾细胞癌相关的失调竞争内源性 RNA 模块。

Detection of dysregulated competing endogenous RNA modules associated with clear cell kidney carcinoma.

机构信息

Network Information Center, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.

College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.

出版信息

Mol Med Rep. 2018 Aug;18(2):1963-1972. doi: 10.3892/mmr.2018.9189. Epub 2018 Jun 19.

DOI:10.3892/mmr.2018.9189
PMID:29956728
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6072225/
Abstract

Recent evidence has suggested that competitive endogenous RNAs (ceRNAs) are important regulatory molecules in clear cell kidney carcinoma (KIRC) and their dysregulation may contribute to cancer pathogenesis. However, the critical roles of dysregulated ceRNAs in KIRC remain unknown. In the present study, a KIRC dysregulated ceRNA‑ceRNA network (KDCCNet) was constructed based on the 'ceRNA hypothesis' by integrating microRNA regulation and expression profiles in cancerous and normal tissues. Two dysregulated patterns of ceRNAs interaction (gain and loss) exist in KDCCNet. The two modules, which are 95% loss interactions and 97% gain interactions, were demonstrated to be able to distinguish normal samples from cancer samples. Two long non‑coding (lnc)‑RNAs (glucuronidase β pseudogene 11 and LIFR antisense RNA 1) demonstrated significant associations with KIRC prognosis. The present study of the KDCCNet revealed a novel biological mechanism for KIRC and provides novel lncRNAs as candidate prognostic biomarkers.

摘要

最近的证据表明,竞争性内源性 RNA(ceRNA)是透明细胞肾细胞癌(KIRC)中的重要调节分子,其失调可能导致癌症发病机制。然而,失调的 ceRNA 在 KIRC 中的关键作用尚不清楚。在本研究中,基于 miRNA 调控和癌组织与正常组织中的表达谱,通过整合“ceRNA 假说”构建了 KIRC 失调的 ceRNA-ceRNA 网络(KDCCNet)。KDCCNet 中存在两种 ceRNA 相互作用的失调模式(增益和缺失)。两个模块,95% 的缺失相互作用和 97% 的增益相互作用,被证明能够区分正常样本和癌症样本。两种长链非编码(lnc)RNAs(β-葡糖苷酸酶假基因 11 和 LIFR 反义 RNA 1)与 KIRC 预后显著相关。本研究的 KDCCNet 揭示了 KIRC 的一种新的生物学机制,并提供了新的 lncRNAs 作为候选预后生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/3f35ea51b283/MMR-18-02-1963-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/ec4272bf1f6a/MMR-18-02-1963-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/d6f572c51846/MMR-18-02-1963-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/31e78e433d55/MMR-18-02-1963-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/336b3fb4fa3d/MMR-18-02-1963-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/3f35ea51b283/MMR-18-02-1963-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/ec4272bf1f6a/MMR-18-02-1963-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/d6f572c51846/MMR-18-02-1963-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/31e78e433d55/MMR-18-02-1963-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/336b3fb4fa3d/MMR-18-02-1963-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/6072225/3f35ea51b283/MMR-18-02-1963-g06.jpg

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