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LINC00467 通过结合 miR-339-3p 促进肌醇六磷酸激酶 2 的表达，促进胶质瘤的增殖、迁移和侵袭。

LINC00467 facilitates the proliferation, migration and invasion of glioma via promoting the expression of inositol hexakisphosphate kinase 2 by binding to miR-339-3p.

机构信息

Department of Neurosurgery, Sir Run Run Hospital, Nanjing Medical University Nanjing, China.

School of Basic Medical Sciences, Nanjing Medical University, Nanjing China.

出版信息

Bioengineered. 2022 Feb;13(2):3370-3382. doi: 10.1080/21655979.2021.2018098.

DOI:10.1080/21655979.2021.2018098
PMID:35156508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8973818/
Abstract

Our previous studies indicate that long noncoding RNA (lncRNA) LINC00467 can act as an oncogene to participate in the malignant progression of glioma, but the underlying molecular mechanism remains to be studied further. This study aimed to explore the biological role of the LINC00467/miR-339-3p/ inositol hexakisphosphate kinase 2 (IP6K2) regulatory axis in glioma. The Cancer Genome Atlas (TCGA), Oncomine databases and reverse transcription‑quantitative PCR (RT‑qPCR) were used to analyze IP6K2 expression in glioma. RT-PCR, EdU and transwell assays were conducted to observe the effect of IP6K2 on glioma cell proliferation, migration and invasion. Using bioinformatics analysis, RT-PCR, and dual luciferase reporter gene assay, the potential role of the LINC00467/miR-339-3p/IP6K2 regulatory axis in glioma was verified. The results showed that IP6K2 was up-regulated in glioma tissues and cell lines. Moreover, the expression level of IP6K2 was correlated with the clinical features of glioma patients. and experiments indicated that IP6K2 overexpression could promote the proliferation, migration, and invasion of glioma cells. Further bioinformatics analysis and assays revealed that LINC00467 could promote IP6K2 expression by binding to miR-339-3p and promote the malignant progression of glioma. Overall, LINC00467 could upregulate IP6K2 by binding to miR-339-3p and promote the proliferation, migration, and invasion of glioma cells. The LINC00467/miR-339-3p/IP6K2 regulatory axis might be a potential therapeutic target for glioma.

摘要

我们之前的研究表明，长链非编码 RNA（lncRNA）LINC00467 可以作为癌基因参与神经胶质瘤的恶性进展，但潜在的分子机制仍需进一步研究。本研究旨在探讨 LINC00467/miR-339-3p/肌醇六磷酸激酶 2（IP6K2）调控轴在神经胶质瘤中的生物学作用。癌症基因组图谱（TCGA）、Oncomine 数据库和逆转录-定量 PCR（RT-qPCR）用于分析神经胶质瘤中 IP6K2 的表达。RT-PCR、EdU 和 Transwell 测定用于观察 IP6K2 对神经胶质瘤细胞增殖、迁移和侵袭的影响。通过生物信息学分析、RT-PCR 和双荧光素酶报告基因检测，验证了 LINC00467/miR-339-3p/IP6K2 调控轴在神经胶质瘤中的潜在作用。结果显示，IP6K2 在神经胶质瘤组织和细胞系中上调。此外，IP6K2 的表达水平与神经胶质瘤患者的临床特征相关。和实验表明，IP6K2 过表达可促进神经胶质瘤细胞的增殖、迁移和侵袭。进一步的生物信息学分析和实验揭示，LINC00467 通过与 miR-339-3p 结合促进 IP6K2 表达，从而促进神经胶质瘤的恶性进展。总之，LINC00467 通过与 miR-339-3p 结合上调 IP6K2，促进神经胶质瘤细胞的增殖、迁移和侵袭。LINC00467/miR-339-3p/IP6K2 调控轴可能是神经胶质瘤的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/d75e8d06f1fc/KBIE_A_2018098_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/a5f31d6f7ee5/KBIE_A_2018098_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/4484482fc5ce/KBIE_A_2018098_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/0b6d870364cb/KBIE_A_2018098_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/44e3a98a614d/KBIE_A_2018098_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/ee2881645fd6/KBIE_A_2018098_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/d75e8d06f1fc/KBIE_A_2018098_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/a5f31d6f7ee5/KBIE_A_2018098_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/4484482fc5ce/KBIE_A_2018098_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/0b6d870364cb/KBIE_A_2018098_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/44e3a98a614d/KBIE_A_2018098_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/ee2881645fd6/KBIE_A_2018098_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dcee/8973818/d75e8d06f1fc/KBIE_A_2018098_F0006_OC.jpg

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