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长链非编码 RNA FTH1P3 通过 microRNA-145 促进宫颈癌的增殖和转移。

The long noncoding RNA FTH1P3 promotes the proliferation and metastasis of cervical cancer through microRNA‑145.

机构信息

Department of Gynecological Oncology Ward, Gansu Provincial Cancer Hospital, Lanzhou, Gansu 730050, P.R. China.

出版信息

Oncol Rep. 2020 Jan;43(1):31-40. doi: 10.3892/or.2019.7413. Epub 2019 Nov 20.

DOI:10.3892/or.2019.7413
PMID:31789421
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6908927/
Abstract

Emerging evidence has revealed that long noncoding RNAs (lncRNAs) play crucial roles in the development and progression of tumors. The present study aimed to examine the roles and illustrate the underlying mechanisms of lncRNA ferritin heavy chain 1 pseudogene 3 (FTH1P3) in cervical cancer. The expression of lncRNA FTH1P3 and microRNA‑145 (miRNA‑145 or miR‑145) in human cervical cancer samples and cervical cancer cell lines was detected by qRT‑PCR (reverse transcription‑quantitative polymerase chain reaction). FTH1P3 overexpression, siRNA plasmid, hsa‑miR‑145 mimic or hsa‑miR‑145 inhibitor were transfected. The target of FTH1P3 was predicted by bioinformatics analysis and validated by luciferase assay. Statistical significance analysis was performed by SPSS software. The results revealed that FTH1P3 was significantly upregulated in cervical cancer tissues compared with normal tissues. Increased expression of FTH1P3 was revealed in human cervical cancer cell lines compared with cervical normal epithelial cells. Downregulation of FTH1P3 inhibited cell proliferation, invasion and migration, and promoted apoptosis in cervical cancer cells. miR‑145 was predicted and validated as a direct target of FTH1P3. Moreover, FTH1P3 siRNA partially attenuated the effects of the miR‑145 inhibitor on cell viability and mobility in cervical cancer cells. The present results demonstrated that lncRNA FTH1P3 functioned as a promoting factor in cervical cancer by targeting miR‑145.

摘要

新出现的证据表明,长非编码 RNA(lncRNA)在肿瘤的发生和发展中起着关键作用。本研究旨在探讨 lncRNA 铁蛋白重链 1 假基因 3(FTH1P3)在宫颈癌中的作用,并阐明其潜在机制。采用 qRT-PCR(反转录-定量聚合酶链反应)检测人宫颈癌组织和宫颈癌细胞系中 lncRNA FTH1P3 和 microRNA-145(miRNA-145 或 miR-145)的表达。转染 FTH1P3 过表达、siRNA 质粒、hsa-miR-145 模拟物或 hsa-miR-145 抑制剂。通过生物信息学分析预测 FTH1P3 的靶标,并通过荧光素酶测定进行验证。采用 SPSS 软件进行统计学意义分析。结果显示,FTH1P3 在宫颈癌组织中的表达明显高于正常组织。FTH1P3 在人宫颈癌细胞系中的表达高于宫颈正常上皮细胞。下调 FTH1P3 抑制宫颈癌细胞的增殖、侵袭和迁移,并促进凋亡。miR-145 被预测并验证为 FTH1P3 的直接靶标。此外,FTH1P3 siRNA 部分减弱了 miR-145 抑制剂对宫颈癌细胞活力和迁移能力的影响。本研究结果表明,lncRNA FTH1P3 通过靶向 miR-145 在宫颈癌中发挥促进因子的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/d82c65e8c6f9/or-43-01-0031-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/4b757bf89591/or-43-01-0031-g00.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/67af9210ce72/or-43-01-0031-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/81719eebad99/or-43-01-0031-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/d82c65e8c6f9/or-43-01-0031-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/4b757bf89591/or-43-01-0031-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/30f54f4317b2/or-43-01-0031-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/73a793cea008/or-43-01-0031-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/be0f5b62c14b/or-43-01-0031-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/67af9210ce72/or-43-01-0031-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/81719eebad99/or-43-01-0031-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f90/6908927/d82c65e8c6f9/or-43-01-0031-g06.jpg

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