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SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381

BACKGROUND: Increasing evidence implies the participation of long non-coding RNAs (lncRNAs) in chemoresistance to cancer treatment. Their role and molecular mechanisms in breast cancer chemoresistance, nevertheless, are yet not considerably elucidated. In this work, we research the function of small...

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Autores principales: Mi, Hailong, Wang, Xiaochun, Wang, Fang, Li, Lin, Zhu, Mingzhi, Wang, Nan, Xiong, Youyi, Gu, Yuanting
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6983676/
https://www.ncbi.nlm.nih.gov/pubmed/32021307
http://dx.doi.org/10.2147/OTT.S223321
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author Mi, Hailong
Wang, Xiaochun
Wang, Fang
Li, Lin
Zhu, Mingzhi
Wang, Nan
Xiong, Youyi
Gu, Yuanting
author_facet Mi, Hailong
Wang, Xiaochun
Wang, Fang
Li, Lin
Zhu, Mingzhi
Wang, Nan
Xiong, Youyi
Gu, Yuanting
author_sort Mi, Hailong
collection PubMed
description BACKGROUND: Increasing evidence implies the participation of long non-coding RNAs (lncRNAs) in chemoresistance to cancer treatment. Their role and molecular mechanisms in breast cancer chemoresistance, nevertheless, are yet not considerably elucidated. In this work, we research the function of small nucleolar RNA host gene 15 (SNHG15) in cisplatin (DDP) resistance of breast cancer and uncover the underlying molecular mechanism. METHODS: SNHG15 and miR-381 expression levels were detected using Quantitative real-time PCR (qRT-PCR) analysis. The functional roles of SNHG15 and miR-381 in breast cancer were determined using MTT assay and flow cytometry analysis. The effect of SNHG15 on miR-381 expression was determined using Luciferase reporter assay, RNA immunoprecipitation (RIP) assay and qRT-PCR analysis. RESULTS: SNHG15 was found to be up-regulated in cisplatin resistant breast cancer tissues and cell lines. Breast cancer patients with high SNHG15 expression had a poor prognosis. SNHG15 silencing enhanced cisplatin sensitivity of MCF-7/DDP and MDA-MB-231/DDP cells. Additionally, SNHG15 could function as a miR-381 sponge. miR-381 overexpression could overcome cisplatin resistance. miR-381 knockdown countered SNHG15 knockdown-mediated enhancement of cisplatin sensitivity in MCF-7/DDP and MDA-MB-231/DDP cells. Besides, SNHG15 knockdown facilitated cisplatin sensitivity of cisplatin resistant breast cancer cells in vivo. CONCLUSION: In summary, SNHG15 knockdown overcame cisplatin resistance of breast cancer by sponging miR-381, providing a novel therapeutic target for breast cancer.
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spelling pubmed-69836762020-02-04 SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381 Mi, Hailong Wang, Xiaochun Wang, Fang Li, Lin Zhu, Mingzhi Wang, Nan Xiong, Youyi Gu, Yuanting Onco Targets Ther Original Research BACKGROUND: Increasing evidence implies the participation of long non-coding RNAs (lncRNAs) in chemoresistance to cancer treatment. Their role and molecular mechanisms in breast cancer chemoresistance, nevertheless, are yet not considerably elucidated. In this work, we research the function of small nucleolar RNA host gene 15 (SNHG15) in cisplatin (DDP) resistance of breast cancer and uncover the underlying molecular mechanism. METHODS: SNHG15 and miR-381 expression levels were detected using Quantitative real-time PCR (qRT-PCR) analysis. The functional roles of SNHG15 and miR-381 in breast cancer were determined using MTT assay and flow cytometry analysis. The effect of SNHG15 on miR-381 expression was determined using Luciferase reporter assay, RNA immunoprecipitation (RIP) assay and qRT-PCR analysis. RESULTS: SNHG15 was found to be up-regulated in cisplatin resistant breast cancer tissues and cell lines. Breast cancer patients with high SNHG15 expression had a poor prognosis. SNHG15 silencing enhanced cisplatin sensitivity of MCF-7/DDP and MDA-MB-231/DDP cells. Additionally, SNHG15 could function as a miR-381 sponge. miR-381 overexpression could overcome cisplatin resistance. miR-381 knockdown countered SNHG15 knockdown-mediated enhancement of cisplatin sensitivity in MCF-7/DDP and MDA-MB-231/DDP cells. Besides, SNHG15 knockdown facilitated cisplatin sensitivity of cisplatin resistant breast cancer cells in vivo. CONCLUSION: In summary, SNHG15 knockdown overcame cisplatin resistance of breast cancer by sponging miR-381, providing a novel therapeutic target for breast cancer. Dove 2020-01-21 /pmc/articles/PMC6983676/ /pubmed/32021307 http://dx.doi.org/10.2147/OTT.S223321 Text en © 2020 Mi et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Mi, Hailong
Wang, Xiaochun
Wang, Fang
Li, Lin
Zhu, Mingzhi
Wang, Nan
Xiong, Youyi
Gu, Yuanting
SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381
title SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381
title_full SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381
title_fullStr SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381
title_full_unstemmed SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381
title_short SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381
title_sort snhg15 contributes to cisplatin resistance in breast cancer through sponging mir-381
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6983676/
https://www.ncbi.nlm.nih.gov/pubmed/32021307
http://dx.doi.org/10.2147/OTT.S223321
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