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Knockdown of lncRNA PCAT6 Enhances Radiosensitivity in Triple-Negative Breast Cancer Cells by Regulating miR-185-5p/TPD52 Axis

Authors Shi R, Wu P, Liu M, Chen B, Cong L

Received 6 November 2019

Accepted for publication 6 February 2020

Published 8 April 2020 Volume 2020:13 Pages 3025—3037

DOI https://doi.org/10.2147/OTT.S237559

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr XuYu Yang


Rui Shi, Peng Wu, Miaomiao Liu, Bing Chen, Longjiao Cong

Liaoning University of Traditional Chinese Medicine, Shenyang 110032, Liaoning, People’s Republic of China

Correspondence: Rui Shi
Liaoning University of Traditional Chinese Medicine, No. 79, Chongshan Road, Huanggu District, Shenyang, Liaoning, People’s Republic of China
Tel +8624 31207114
Email decvnk@163.com

Background: Long non-coding RNAs (lncRNAs) have been reported to play essential roles in regulating the radiosensitivity of cancers. Prostate cancer-associated transcript 6 (PCAT6) exerts oncogenic roles in several tumors. However, the roles of PCAT6 and its underlying mechanism in regulating the radiosensitivity of triple-negative breast cancer (TNBC) have not been investigated.
Methods: The expression levels of PCAT6, microRNA-185-5p (miR-185-5p) and tumor protein D52 (TPD52) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis and colony formation were assessed by Cell Counting Kit-8 (CCK-8) assay, flow cytometry and colony formation assay, respectively. The interaction between miR-185-5p and PCAT6 or TPD52 was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. Western blot was carried out to detect the protein level of TPD52.
Results: PCAT6 and TPD52 were highly expressed and miR-185-5p was lowly expressed in TNBC tissues and cells, which was associated with an aggressive tumor phenotype in patients, affecting lymph node metastasis and clinical stage. PCAT6 or TPD52 knockdown or miR-185-5p overexpression enhanced the radiosensitivity of TNBC cells via inhibiting proliferation and inducing apoptosis. PCAT6 directly interacted with miR-185-5p and negatively regulated miR-185-5p expression. Moreover, TPD52 was confirmed as a target of miR-185-5p. Besides, PCAT6 regulated the radiosensitivity of TNBC cells through acting as a molecular sponge of miR-185-5p to modulate TPD52 expression.
Conclusion: Knockdown of PCAT6 promoted the radiosensitivity of TNBC cells through regulating miR-185-5p/TPD52 axis, providing a vital theoretical basis to improve the radiotherapy efficiency of TNBC.

Keywords: triple-negative breast cancer, PCAT6, miR-185-5p, TPD52, radiosensitivity

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