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Cancer Manag Res. 2018 Oct 11;10:4371-4380. doi: 10.2147/CMAR.S171126. eCollection 2018.

Non-coding RNA NEAT1/miR-214-3p contribute to doxorubicin resistance of urothelial bladder cancer preliminary through the Wnt/β-catenin pathway.

Guo Y1,2,3, Zhang H4, Xie D5, Hu X6, Song R1,2,3, Zhu L1,2,3.

Author information

1
Department of Central Laboratory, School of Stomatology, China Medical University, Shenyang, Liaoning, People's Republic of China, yguo@cmu.edu.cn.
2
Key Laboratory of Oral Disease of Liaoning Province, Shenyang, Liaoning, People's Republic of China, yguo@cmu.edu.cn.
3
Department of Oral Biology, School of Stomatology, China Medical University, Shenyang, Liaoning, People's Republic of China, yguo@cmu.edu.cn.
4
Department of Urinary Surgery, Shengjing Hospital, China Medical University, Shenyang, People's Republic of China.
5
Department of Anatomy, College of Basic Medicine, China Medical University, Shenyang, People's Republic of China.
6
Department of Neurobiology, China Medical University, Shenyang, Liaoning, People's Republic of China.

Abstract

Background:

Urothelial bladder cancer (UBC) is one of the most lethal urological malignancies in the world. Patients with UBC are routinely given chemotherapy which results in a median survival of 12-15 months. Nuclear-enriched abundant transcript 1 (NEAT1) functions as an oncogene and could be used as a therapeutic target for human UBC. However, the involvement of NEAT1 in doxorubicin (DOX) resistance of UBC has been poorly demonstrated.

Methods:

Quantitative Real-time PCR (qRT-PCR) was used to detect the expression levels of NEAT1 and miR-214-3p in UBC tissues and cells. Bioinformatics prediction, RNA pull-down and qRT-PCR were used to assay the regulation manner of NEAT1 and miR-214-3p. Loss/gain function of NEAT1 and miR-214-3p together with western blot, drug resistance assay and flow cytometry were used to explore the influence of NEAT1 in DOX resistance was correlative with miR-214-3p. Finally, luciferase assay system was applied to determine the Wnt/β-catenin signal activity.

Results:

NEAT1 was upregulated and miR-214-3p was downregulated in DOX-resistant UBC tissues and cells. NEAT1 knockdown inhibited J82 and T24 cells to DOX chemosensitivity by negatively regulating miR-214-3p expression. NEAT1/miR-214-3p contributed to DOX resistance of UBC preliminary through the Wnt/β-catenin pathway.

Conclusion:

NEAT1 contributed to DOX resistance of UBC through the Wnt/β-catenin pathway partly by negatively regulating miR-214-3p expression. Our findings will provide a promising ncRNA targeted therapeutic strategy for UBC with DOX resistance.

KEYWORDS:

Wnt/β-catenin pathway; doxorubicin resistance; miR-214-3p; nuclear-enriched abundant transcript 1; urothelial bladder cancer

Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

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