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长链非编码 RNA Linc00485 通过调节 miR-298/c-Myc 轴促进肺癌进展。

Long intergenic non-coding RNA Linc00485 promotes lung cancer progression by modulating miR-298/c-Myc axis.

机构信息

Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.

School of Stomatology, Fujian Medical University, Fuzhou, Fujian, China.

出版信息

J Cell Mol Med. 2021 Jan;25(1):309-322. doi: 10.1111/jcmm.16036. Epub 2020 Nov 25.

DOI:10.1111/jcmm.16036
PMID:33237626
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7810966/
Abstract

Long non-coding RNAs (lncRNAs), which are non-protein-coding transcripts, are emerging as novel biomarkers for cancer diagnosis. Their dysregulation is increasingly recognized to contribute to the development and progression of human cancers, including lung cancer. Linc00485 is a newly discovered cancer-related lncRNA; however, little is known about its role in lung cancer progression. In this study, we found that the expression of Linc00485 was significantly increased in human lung cancer tissue and associated with malignant phenotypes, including tumour-node-metastasis (TNM) stage, metastasis and relapse. Furthermore, the proliferative, migratory and invasive abilities of lung cancer cells in vitro were significantly enhanced by overexpression of Linc00485 but inhibited by its silencing. Mechanistically, Linc00485 regulated the expression of c-Myc by directly binding to miR-298; the effects of Linc00485 overexpression could be significantly reversed by a c-Myc inhibitor or small interfering RNA. Xenotransplantation experiments showed that Linc00485 silencing significantly weakened the proliferation potential of A549 cells in vivo. Overall, these findings indicate that Linc00485 overexpression down-regulates miR-298, resulting in the up-regulation of c-Myc and thereby promoting the development of lung cancer.

摘要

长非编码 RNA（lncRNA）是一类不编码蛋白质的转录本，作为癌症诊断的新型生物标志物而受到关注。它们的失调被认为越来越多地导致人类癌症的发展和进展，包括肺癌。Linc00485 是一种新发现的与癌症相关的 lncRNA；然而，其在肺癌进展中的作用知之甚少。在这项研究中，我们发现 Linc00485 在人类肺癌组织中的表达显著增加，并且与恶性表型相关，包括肿瘤-淋巴结-转移（TNM）分期、转移和复发。此外，Linc00485 的过表达显著增强了肺癌细胞在体外的增殖、迁移和侵袭能力，而其沉默则抑制了这些能力。机制上，Linc00485 通过直接结合 miR-298 来调节 c-Myc 的表达；c-Myc 抑制剂或小干扰 RNA 可显著逆转 Linc00485 过表达的作用。异种移植实验表明，Linc00485 沉默显著减弱了 A549 细胞在体内的增殖潜力。总之，这些发现表明 Linc00485 的过表达下调了 miR-298，导致 c-Myc 的上调，从而促进了肺癌的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee68/7810966/80d1d0be5413/JCMM-25-309-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee68/7810966/f583893289ec/JCMM-25-309-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee68/7810966/7f19da6bc9b8/JCMM-25-309-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee68/7810966/c389f6df8ce0/JCMM-25-309-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee68/7810966/80d1d0be5413/JCMM-25-309-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee68/7810966/f583893289ec/JCMM-25-309-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee68/7810966/be2e990970a5/JCMM-25-309-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee68/7810966/d4d038d4b66e/JCMM-25-309-g003.jpg
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