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长链非编码 RNA LINC01296 通过海绵吸附 miR-5095 促进人胆管癌的肿瘤生长和进展。

Long noncoding RNA LINC01296 promotes tumor growth and progression by sponging miR-5095 in human cholangiocarcinoma.

机构信息

Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510260, P.R. China.

Department of Breast and Thyroid Surgery, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510655, P.R. China.

出版信息

Int J Oncol. 2018 Jun;52(6):1777-1786. doi: 10.3892/ijo.2018.4362. Epub 2018 Apr 5.

DOI:10.3892/ijo.2018.4362
PMID:29620172
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5919714/
Abstract

The aim of the present study was to elucidate whether, and how, long intergenic non-protein coding RNA 1296 (LINC01296) is involved in the modulation of human cholangiocarcinoma (CCA) development and progression. Microarray data analysis and reverse transcription-quantitative polymerase chain reaction analysis demonstrated that LINC01296 was significantly upregulated in human CCA compared with nontumor tissues. Furthermore, the expression of LINC01296 in human CCA was positively associated with tumor severity and clinical stage. Knockdown of LINC01296 dramatically suppressed the viability, migration and invasion of RBE and CCLP1 cells, and promoted cell apoptosis in vitro. Furthermore, LINC01296 knockdown inhibited tumor growth in a xenograft model. Mechanistically, LINC01296 was demonstrated to sponge microRNA-5095 (miR-5095), which targets MYCN proto-oncogene bHLH transcription factor (MYCN) mRNA in human CCA. By inhibition of miR-5095, LINC01296 overexpression upregulated the expression of MYCN and promoted cell viability, migration and invasion in CCA cells. The results reveal that the axis of LINC01296/miR-5095/MYCN may be a mechanism to regulate CCA development and progression.

摘要

本研究旨在阐明长链非编码 RNA 1296（LINC01296）是否以及如何参与调节人类胆管癌（CCA）的发生和发展。微阵列数据分析和逆转录定量聚合酶链反应分析表明，LINC01296 在人 CCA 组织中明显上调，与非肿瘤组织相比。此外，LINC01296 在人 CCA 中的表达与肿瘤严重程度和临床分期呈正相关。LINC01296 敲低显著抑制了 RBE 和 CCLP1 细胞的活力、迁移和侵袭，并促进了体外细胞凋亡。此外，LINC01296 敲低抑制了异种移植模型中的肿瘤生长。机制上，LINC01296 被证明可以海绵 microRNA-5095（miR-5095），miR-5095 在人类 CCA 中靶向 MYCN 原癌基因 bHLH 转录因子（MYCN）mRNA。通过抑制 miR-5095，LINC01296 的过表达上调了 MYCN 的表达，并促进了 CCA 细胞的活力、迁移和侵袭。研究结果表明，LINC01296/miR-5095/MYCN 轴可能是调节 CCA 发生和发展的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/f354fea40886/IJO-52-06-1777-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/f08c2dfe3a2e/IJO-52-06-1777-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/816cd04a5767/IJO-52-06-1777-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/6bfa5b8902f6/IJO-52-06-1777-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/6a688b5f48a6/IJO-52-06-1777-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/89839809e80a/IJO-52-06-1777-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/e8c7515c8a0c/IJO-52-06-1777-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/f354fea40886/IJO-52-06-1777-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/f08c2dfe3a2e/IJO-52-06-1777-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/816cd04a5767/IJO-52-06-1777-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/6bfa5b8902f6/IJO-52-06-1777-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/6a688b5f48a6/IJO-52-06-1777-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/89839809e80a/IJO-52-06-1777-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/e8c7515c8a0c/IJO-52-06-1777-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6991/5919714/f354fea40886/IJO-52-06-1777-g06.jpg

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