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长链非编码RNA通过下调miR34a甲基化促进视网膜母细胞瘤细胞增殖。

lncRNA Promotes the Proliferation of Retinoblastoma Cells Through Downregulating miR34a Methylation.

作者信息

Yang Bo, Gu Baoyu, Zhang Jing, Xu Long, Sun Yong

机构信息

Department of Ophthalmology, Shenzhen Hospital of Integrated Chinese and Western Medicine, Shenzhen 518101, Guangdong Province, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Dec 30;12:13461-13467. doi: 10.2147/CMAR.S268380. eCollection 2020.

DOI:10.2147/CMAR.S268380
PMID:33408518
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7779858/
Abstract

BACKGROUND: lncRNA has been proven to be oncogenic in a variety of cancers, but its role in other types of cancer remains unclear. This study was to investigate the role of in retinoblastoma (Rb). METHODS: RT-qPCR was performed to determine the expression of and miR34a in paired Rb and nontumor tissue. Overexpression of and miR34a in Rb cells was achieved to evaluate the interaction between them. Methylation-specific PCR was used to analyze the effect of overexpression on gene methylation. CCK8 assays were used to analyze cell proliferation. RESULTS: The results showed that expression was upregulated and miR34a expression downregulated in Rb tissue. Moreover, miR34a expression was negatively correlated with the of expression in Rb tissue. Overexpression of decreased expression of miR34a and increased methylation of in Rb cells. In addition, overexpression of reduced the inhibitory effects of miR34a on Rb-cell proliferation. CONCLUSION: may promote Rb cell proliferation by downregulating miR34a methylation.

摘要

背景：长链非编码RNA（lncRNA）已被证实在多种癌症中具有致癌作用，但其在其他类型癌症中的作用仍不清楚。本研究旨在探讨lncRNA在视网膜母细胞瘤（Rb）中的作用。 方法：采用逆转录定量聚合酶链反应（RT-qPCR）检测lncRNA和miR34a在配对的Rb组织和非肿瘤组织中的表达。通过在Rb细胞中过表达lncRNA和miR34a来评估它们之间的相互作用。采用甲基化特异性PCR分析lncRNA过表达对miR34a基因甲基化的影响。使用细胞计数试剂盒-8（CCK8）分析细胞增殖情况。 结果：结果显示，Rb组织中lncRNA表达上调，miR34a表达下调。此外，Rb组织中miR34a表达与lncRNA表达呈负相关。lncRNA过表达降低了Rb细胞中miR34a的表达，并增加了miR34a的甲基化。此外，lncRNA过表达减弱了miR34a对Rb细胞增殖的抑制作用。 结论：lncRNA可能通过下调miR34a甲基化促进Rb细胞增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50e/7779858/c6d6decb1973/CMAR-12-13461-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50e/7779858/24c40177a324/CMAR-12-13461-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50e/7779858/413c7d78d764/CMAR-12-13461-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50e/7779858/7edaad138991/CMAR-12-13461-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50e/7779858/c6d6decb1973/CMAR-12-13461-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50e/7779858/24c40177a324/CMAR-12-13461-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50e/7779858/413c7d78d764/CMAR-12-13461-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50e/7779858/7edaad138991/CMAR-12-13461-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c50e/7779858/c6d6decb1973/CMAR-12-13461-g0004.jpg

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[9]
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本文引用的文献

[1]
Non-Coding RNAs in Retinoblastoma.

Front Genet. 2019-11-14

[2]
Association of lncRNA and Gene Polymorphisms with Hepatocellular Carcinoma.

Int J Environ Res Public Health. 2019-8-8

[3]
Therapeutic targeting of the RB1 pathway in retinoblastoma with the oncolytic adenovirus VCN-01.

Sci Transl Med. 2019-1-23

[4]
miR‑34a regulates the chemosensitivity of retinoblastoma cells via modulation of MAGE‑A/p53 signaling.

Int J Oncol. 2019-1

[5]
Shikonin-mediated up-regulation of miR-34a and miR-202 inhibits retinoblastoma proliferation.

Toxicol Res (Camb). 2018-6-6

[6]
Association between lncRNA CASC8 polymorphisms and the risk of cancer: a meta-analysis.

Cancer Manag Res. 2018-8-31

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Characterization and Molecular Mechanism of Peptide-Conjugated Gold Nanoparticle Inhibiting p53-HDM2 Interaction in Retinoblastoma.

Mol Ther Nucleic Acids. 2017-12-15

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Metastatic deaths in retinoblastoma patients treated with intraarterial chemotherapy (ophthalmic artery chemosurgery) worldwide.

Int J Retina Vitreous. 2017-10-23

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Alternative mechanisms of miR-34a regulation in cancer.

Cell Death Dis. 2017-10-12

[10]
Association of lnc-LAMC2-1:1 rs2147578 and CASC8 rs10505477 Polymorphisms with Risk of Childhood Acute Lymphoblastic Leukemia.

Asian Pac J Cancer Prev. 2016-11-1

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