Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of miR-27b-3p and Subsequently Increasing ATF2 Expression

Lei Li, Guohua Lv, Bing Wang, Hong Ma Department of Spine Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, People’s Republic of ChinaCorrespondence: Hong Ma Tel +86 731-85295124Email spinema@csu.edu.cnBackground: Chordoma, a rare bone tumor, occurs mo...

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Main Authors: Li L, Lv G, Wang B, Ma H
Format: Article
Language:English
Published: Dove Medical Press 2020-08-01
Series:Cancer Management and Research
Subjects:
mdr
Online Access:https://www.dovepress.com/long-non-coding-rna-kcnq1ot1-promotes-multidrug-resistance-in-chordoma-peer-reviewed-article-CMAR
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spelling doaj-b717b5e0326948eda9d71d3a1223d6622020-11-25T03:42:27ZengDove Medical PressCancer Management and Research1179-13222020-08-01Volume 127847785356624Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of miR-27b-3p and Subsequently Increasing ATF2 ExpressionLi LLv GWang BMa HLei Li, Guohua Lv, Bing Wang, Hong Ma Department of Spine Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, People’s Republic of ChinaCorrespondence: Hong Ma Tel +86 731-85295124Email spinema@csu.edu.cnBackground: Chordoma, a rare bone tumor, occurs most commonly at the sacrococcygeal and skull base region. To date, chemotherapy is used to treat patients with advanced-stage chordoma. However, multidrug resistance (MDR) greatly hinders the effect of chemotherapy in chordoma. Here, we studied the correlation between KCNQ1OT1 and chemotherapy resistance.Methods: RT-PCR assay was used to examine KCNQ1OT1, miR-27b-3p, and ATF2 mRNA expression. CCK8 assay was exercised to detect IC50 values of cisplatin in chordoma cells. ATF2 protein expression was detected by Western blot.Results: KCNQ1OT1 was increased in chemotherapy-resistant patients and cisplatin-resistant cells, and downregulation of KCNQ1OT1 expression weakened MDR in chordoma. In addition, KCNQ1OT1 promoted MDR in chordoma by sponging miR-27b-3p and subsequently increasing ATF2 expression.Conclusion: KCNQ1OT1 is proved to be strikingly raised in the chemotherapy-resistant group and to promote MDR in chordoma. Our findings demonstrated the role of the KCNQ1OT1/miR-27b-3p/ATF2 axis in MDR of chordoma, which provides new insight into the molecular mechanism of chordoma MDR, and may determine the effect of therapy after receiving chemotherapy by detecting the expression of KCNQ1OT1 in serum.Keywords: KCNQ1OT1, MDR, miR-27b-3p, ATF2, chordomahttps://www.dovepress.com/long-non-coding-rna-kcnq1ot1-promotes-multidrug-resistance-in-chordoma-peer-reviewed-article-CMARkcnq1ot1mdrmir-27b-3patf2chordoma
collection DOAJ
language English
format Article
sources DOAJ
author Li L
Lv G
Wang B
Ma H
spellingShingle Li L
Lv G
Wang B
Ma H
Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of miR-27b-3p and Subsequently Increasing ATF2 Expression
Cancer Management and Research
kcnq1ot1
mdr
mir-27b-3p
atf2
chordoma
author_facet Li L
Lv G
Wang B
Ma H
author_sort Li L
title Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of miR-27b-3p and Subsequently Increasing ATF2 Expression
title_short Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of miR-27b-3p and Subsequently Increasing ATF2 Expression
title_full Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of miR-27b-3p and Subsequently Increasing ATF2 Expression
title_fullStr Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of miR-27b-3p and Subsequently Increasing ATF2 Expression
title_full_unstemmed Long Non-Coding RNA KCNQ1OT1 Promotes Multidrug Resistance in Chordoma by Functioning as a Molecular Sponge of miR-27b-3p and Subsequently Increasing ATF2 Expression
title_sort long non-coding rna kcnq1ot1 promotes multidrug resistance in chordoma by functioning as a molecular sponge of mir-27b-3p and subsequently increasing atf2 expression
publisher Dove Medical Press
series Cancer Management and Research
issn 1179-1322
publishDate 2020-08-01
description Lei Li, Guohua Lv, Bing Wang, Hong Ma Department of Spine Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, People’s Republic of ChinaCorrespondence: Hong Ma Tel +86 731-85295124Email spinema@csu.edu.cnBackground: Chordoma, a rare bone tumor, occurs most commonly at the sacrococcygeal and skull base region. To date, chemotherapy is used to treat patients with advanced-stage chordoma. However, multidrug resistance (MDR) greatly hinders the effect of chemotherapy in chordoma. Here, we studied the correlation between KCNQ1OT1 and chemotherapy resistance.Methods: RT-PCR assay was used to examine KCNQ1OT1, miR-27b-3p, and ATF2 mRNA expression. CCK8 assay was exercised to detect IC50 values of cisplatin in chordoma cells. ATF2 protein expression was detected by Western blot.Results: KCNQ1OT1 was increased in chemotherapy-resistant patients and cisplatin-resistant cells, and downregulation of KCNQ1OT1 expression weakened MDR in chordoma. In addition, KCNQ1OT1 promoted MDR in chordoma by sponging miR-27b-3p and subsequently increasing ATF2 expression.Conclusion: KCNQ1OT1 is proved to be strikingly raised in the chemotherapy-resistant group and to promote MDR in chordoma. Our findings demonstrated the role of the KCNQ1OT1/miR-27b-3p/ATF2 axis in MDR of chordoma, which provides new insight into the molecular mechanism of chordoma MDR, and may determine the effect of therapy after receiving chemotherapy by detecting the expression of KCNQ1OT1 in serum.Keywords: KCNQ1OT1, MDR, miR-27b-3p, ATF2, chordoma
topic kcnq1ot1
mdr
mir-27b-3p
atf2
chordoma
url https://www.dovepress.com/long-non-coding-rna-kcnq1ot1-promotes-multidrug-resistance-in-chordoma-peer-reviewed-article-CMAR
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