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长链非编码RNA FTH1P3通过miR-224-5p促进葡萄膜黑色素瘤细胞的生长和侵袭。

Long non-coding RNA FTH1P3 facilitates uveal melanoma cell growth and invasion through miR-224-5p.

作者信息

Zheng Xiaoli, Tang Hongwei, Zhao Xiaofeng, Sun Yamei, Jiang Yanfang, Liu Yonghua

机构信息

Department of Ophthalmology, Liaocheng People's Hospital, Liaocheng, Shandong, China.

Joint Laboratory for Translational Medicine, Liaocheng People's Hospital, Liaocheng, Shandong, China.

出版信息

PLoS One. 2017 Nov 2;12(11):e0184746. doi: 10.1371/journal.pone.0184746. eCollection 2017.

DOI:10.1371/journal.pone.0184746
PMID:29095823
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5667836/
Abstract

Growing evidences indicated that Long noncoding RNAs (lncRNAs) played important roles in tumor initiation and progression. However, the function and mechnism of lncRNA ferritin heavy chain 1 pseudogene 3 (FTH1P3) remain unknown in uveal melanoma. We showed that the expression level of FTH1P3 was upregulated in uveal melanoma cell lines and tissues. Elevated expression of FTH1P3 promoted uveal melanoma cell proliferation, cell cycle and migration. Moreover, we found that FTH1P3 was a direct target gene of miR-224-5p in uveal melanoma cell. Overexpression of FTH1P3 suppressed miR-224-5p expression and promoted the expression of Rac1 and Fizzled 5, which were the direct target genes of miR-224-5p. Furthermore, we showed that miR-224-5p expression level was downregulated in uveal melanoma cell lines and tissues. FTH1P3 expression was inversely correlated with the miR-224-5p expression in uveal melanoma tissues. Ectopic expression of miR-224-5p decreased uveal melanoma cell proliferation, cell cycle and migration. Elevated expression of FTH1P3 enhanced uveal melanoma cell proliferation and migration by inhibiting miR-224-5p expression. These results suggest that lncRNA FTH1P3 plays a crucial role in uveal melanoma. Investigation of the underlying mechanism may be a target for the treatment of uveal melanoma.

摘要

越来越多的证据表明，长链非编码RNA（lncRNAs）在肿瘤的发生和发展中发挥着重要作用。然而，lncRNA铁蛋白重链1假基因3（FTH1P3）在葡萄膜黑色素瘤中的功能和机制尚不清楚。我们发现FTH1P3在葡萄膜黑色素瘤细胞系和组织中的表达水平上调。FTH1P3表达的升高促进了葡萄膜黑色素瘤细胞的增殖、细胞周期进程和迁移。此外，我们发现FTH1P3是葡萄膜黑色素瘤细胞中miR-224-5p的直接靶基因。FTH1P3的过表达抑制了miR-224-5p的表达，并促进了Rac1和Fizzled 5的表达，而这两个基因是miR-224-5p的直接靶基因。此外，我们发现miR-224-5p在葡萄膜黑色素瘤细胞系和组织中的表达水平下调。在葡萄膜黑色素瘤组织中，FTH1P3的表达与miR-224-5p的表达呈负相关。miR-224-5p的异位表达降低了葡萄膜黑色素瘤细胞的增殖、细胞周期进程和迁移。FTH1P3表达的升高通过抑制miR-224-5p的表达增强了葡萄膜黑色素瘤细胞 的增殖和迁移。这些结果表明lncRNA FTH1P3在葡萄膜黑色素瘤中起关键作用。对其潜在机制的研究可能是治疗葡萄膜黑色素瘤的一个靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/5083b0c2b526/pone.0184746.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/a34151e98619/pone.0184746.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/df7e4ab77af4/pone.0184746.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/a3f81c898bd1/pone.0184746.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/69f8cdd09c02/pone.0184746.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/87d8979b84d2/pone.0184746.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/5083b0c2b526/pone.0184746.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/a34151e98619/pone.0184746.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/df7e4ab77af4/pone.0184746.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/a3f81c898bd1/pone.0184746.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/69f8cdd09c02/pone.0184746.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/87d8979b84d2/pone.0184746.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/5667836/5083b0c2b526/pone.0184746.g006.jpg

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