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EIF3J-AS1通过海绵化miR-1343-3p上调膜联蛋白A11来促进胶质瘤细胞生长。

EIF3J-AS1 promotes glioma cell growth via up-regulating ANXA11 through sponging miR-1343-3p.

作者信息

Qi Jianguo, Wang Zhengrui, Zhao Zhensheng, Liu Lijun

机构信息

Department of Neurosuigery, The Third People's Hospital of Jinan, Jinan, 250101 Shandong China.

Department of Neurosurgery, Chengyang People's Hospital of Qingdao, Qingdao, 266109 Shandong China.

出版信息

Cancer Cell Int. 2020 Sep 3;20:428. doi: 10.1186/s12935-020-01487-2. eCollection 2020.

DOI:10.1186/s12935-020-01487-2
PMID:32905397
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7469350/
Abstract

BACKGROUND

Glioma is one prevalent malignant tumor originates from the central nervous system. Dysregulation of long non-coding RNAs (lncRNAs) has been found to be a molecular signature behind the pathology of a variety of cancers, including glioma. EIF3J antisense RNA 1 (EIF3J-AS1) is a novel lncRNA, whose performance in carcinogenesis has been unfolded. Nevertheless, the role of EIF3J-AS1 has never been investigated in glioma.

METHODS

qRT-PCR analysis was adopted to evaluate the relative levels of RNAs. In vitro functional assays, including colony formation, EdU, TUNEL and caspase-3/8/9 activity assays were conducted to study the impacts of EIF3J-AS1 on glioma. Dual-luciferase activity assays, RNA pull down assay and RIP assay were performed to elucidate molecular interplay among genes.

RESULTS

EIF3J-AS1 was overexpressed in glioma cell lines. Knockdown of EIF3J-AS1 hampered glioma malignant phenotypes. MiR-1343-3p could bind to EIF3J-AS1. Moreover, miR-1343-3p targeted Annexin A11 (ANXA11) in its 3'UTR region. Mechanistically, EIF3J-AS1 relieved ANXA11 from miR-1343-3p silencing in the EIF3J-AS1/miR-1343-3p/ANXA11 RNA induced silencing complex (RISC), thus eliciting promoting effects on glioma progression. MiR-1343-3p inhibitor and ANXA11 overexpression offset the inhibitory impacts of EIF3J-AS1 silencing on glioma development.

CONCLUSION

EIF3J-AS1/miR-1343-3p/ANXA11 axis significantly affected biological behaviors in glioma, suggesting new therapeutic target for glioma treatment.

摘要

背景

胶质瘤是一种常见的起源于中枢神经系统的恶性肿瘤。长链非编码RNA（lncRNA）失调已被发现是包括胶质瘤在内的多种癌症病理背后的分子特征。EIF3J反义RNA 1（EIF3J-AS1）是一种新型lncRNA，其在致癌过程中的作用已被揭示。然而，EIF3J-AS1在胶质瘤中的作用从未被研究过。

方法

采用qRT-PCR分析评估RNA的相对水平。进行体外功能试验，包括集落形成、EdU、TUNEL和caspase-3/8/9活性试验，以研究EIF3J-AS1对胶质瘤的影响。进行双荧光素酶活性试验、RNA下拉试验和RIP试验，以阐明基因之间的分子相互作用。

结果

EIF3J-AS1在胶质瘤细胞系中过表达。敲低EIF3J-AS1可阻碍胶质瘤的恶性表型。MiR-1343-3p可与EIF3J-AS1结合。此外，miR-1343-3p在其3'UTR区域靶向膜联蛋白A11（ANXA11）。机制上，EIF3J-AS1在EIF3J-AS1/miR-1343-3p/ANXA11 RNA诱导沉默复合体（RISC）中使ANXA11从miR-1343-3p沉默中解脱出来，从而对胶质瘤进展产生促进作用。MiR-1343-3p抑制剂和ANXA11过表达抵消了EIF3J-AS1沉默对胶质瘤发展的抑制作用。

结论

EIF3J-AS1/miR-1343-3p/ANXA11轴显著影响胶质瘤的生物学行为，为胶质瘤治疗提供了新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/31cab542ab46/12935_2020_1487_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/92fee6ae5194/12935_2020_1487_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/72bfc4a1a180/12935_2020_1487_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/b2c9b56fece4/12935_2020_1487_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/7b8c4e11f64b/12935_2020_1487_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/0db4d2479019/12935_2020_1487_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/31cab542ab46/12935_2020_1487_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/92fee6ae5194/12935_2020_1487_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/72bfc4a1a180/12935_2020_1487_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/b2c9b56fece4/12935_2020_1487_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/7b8c4e11f64b/12935_2020_1487_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/0db4d2479019/12935_2020_1487_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20e1/7469350/31cab542ab46/12935_2020_1487_Fig6_HTML.jpg

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