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肺癌中miR-31宿主基因位点的等位基因失衡——其在致癌作用中的潜在作用。

Allelic imbalance in the miR-31 host gene locus in lung cancer--its potential role in carcinogenesis.

作者信息

Okudela Koji, Tateishi Yoko, Umeda Shigeaki, Mitsui Hideaki, Suzuki Takeshisa, Saito Yuichi, Woo Tetsukan, Tajiri Michihiko, Masuda Munetaka, Miyagi Yohei, Ohashi Kenichi

机构信息

Department of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Department of Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

出版信息

PLoS One. 2014 Jun 30;9(6):e100581. doi: 10.1371/journal.pone.0100581. eCollection 2014.

DOI:10.1371/journal.pone.0100581
PMID:24978700
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4076198/
Abstract

Small non-protein coding RNA, microRNA (miR), which regulate messenger RNA levels, have recently been identified, and may play important roles in the pathogenesis of various diseases. The present study focused on miR-31 and investigated its potential involvement in lung carcinogenesis. The expression of miR-31 was altered in lung cancer cells through either the amplification or loss of the host gene locus. The strong expression of miR-31 in large cell carcinomas was attributed to the gene amplification. Meanwhile, the loss of miR-31 expression was more frequently observed in aggressive adenocarcinomas. Thus, miR-31 may play a pleiotropic role in the development of lung cancers among different histological types. To the best of our knowledge, this is the first study to show the potential causative mechanism of the altered expression of miR-31 and suggest its potentially diverse significance in the different histological types of lung cancers.

摘要

小的非蛋白质编码RNA,即微小RNA(miR),可调节信使RNA水平,最近已被发现,并且可能在各种疾病的发病机制中发挥重要作用。本研究聚焦于miR-31,并研究了其在肺癌发生中的潜在作用。miR-31的表达在肺癌细胞中通过宿主基因位点的扩增或缺失而发生改变。miR-31在大细胞癌中的高表达归因于基因扩增。同时,miR-31表达缺失在侵袭性腺癌中更常见。因此,miR-31可能在不同组织学类型的肺癌发生中发挥多效性作用。据我们所知,这是第一项揭示miR-31表达改变潜在致病机制并表明其在不同组织学类型肺癌中可能具有不同意义的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/d8e0c53f8601/pone.0100581.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/024901f59e93/pone.0100581.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/53c3533a8278/pone.0100581.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/83f64120c846/pone.0100581.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/2ae991f87f1c/pone.0100581.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/d8e0c53f8601/pone.0100581.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/024901f59e93/pone.0100581.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/53c3533a8278/pone.0100581.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/83f64120c846/pone.0100581.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/2ae991f87f1c/pone.0100581.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e28/4076198/d8e0c53f8601/pone.0100581.g006.jpg

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