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Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis

Long non-coding RNA (lncRNA) second chromosome locus associated with prostate-1 (SChLAP1), also named LINC00913, has been reported to accelerate the carcinogenesis of prostate cancer. The aim of this study was to explore the role and mechanism of SChLAP1 in triple negative breast cancer (TNBC). The...

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Autores principales: Bai, Xiangdong, Zhang, Shengxiao, Qiao, Jun, Xing, Xiaolong, Li, Weina, Zhang, Huanhu, Xie, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8060801/
https://www.ncbi.nlm.nih.gov/pubmed/33846810
http://dx.doi.org/10.3892/mmr.2021.12085
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author Bai, Xiangdong
Zhang, Shengxiao
Qiao, Jun
Xing, Xiaolong
Li, Weina
Zhang, Huanhu
Xie, Jun
author_facet Bai, Xiangdong
Zhang, Shengxiao
Qiao, Jun
Xing, Xiaolong
Li, Weina
Zhang, Huanhu
Xie, Jun
author_sort Bai, Xiangdong
collection PubMed
description Long non-coding RNA (lncRNA) second chromosome locus associated with prostate-1 (SChLAP1), also named LINC00913, has been reported to accelerate the carcinogenesis of prostate cancer. The aim of this study was to explore the role and mechanism of SChLAP1 in triple negative breast cancer (TNBC). The expression of SChLAP1 in TNBC tissues and cells was determined by reverse transcription quantitative PCR. The effects of SChLAP1 on the growth of TNBC cells was evaluated by detecting cell viability, colony formation and apoptosis. The present study determined that SChLAP1 was upregulated in TNBC tissues and was associated with the long-distant lymph node metastasis of patients with TNBC. Knockdown of SChLAP1 significantly inhibited cell viability and colony formation, and triggered apoptosis of TNBC cells. Bioinformatics analysis suggested that SChLAP1 acted as a sponge of microRNA (miR)-524-5p and negatively modulated the expression of miR-524-5p. An inverse correlation was also identified between the expression levels of SChLAP1 and miR-524-5p in TNBC tissues. Furthermore, the results demonstrated that SChLAP1 interacted with miR-524-5p, and subsequently regulated the expression level of High Mobility Group AT-Hook 2 (HMGA2) in TNBC cells. It was also found that the overexpression of HMGA2 rescued the suppressed viability of TNBC cells induced by SChLAP1 knockdown. In conclusion, the present findings demonstrated that SChLAP1 modulated the malignant tumor behaviors of TNBC cells by regulating HMGA2 and subsequently restraining miR-524-5p.
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spelling pubmed-80608012021-04-25 Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis Bai, Xiangdong Zhang, Shengxiao Qiao, Jun Xing, Xiaolong Li, Weina Zhang, Huanhu Xie, Jun Mol Med Rep Articles Long non-coding RNA (lncRNA) second chromosome locus associated with prostate-1 (SChLAP1), also named LINC00913, has been reported to accelerate the carcinogenesis of prostate cancer. The aim of this study was to explore the role and mechanism of SChLAP1 in triple negative breast cancer (TNBC). The expression of SChLAP1 in TNBC tissues and cells was determined by reverse transcription quantitative PCR. The effects of SChLAP1 on the growth of TNBC cells was evaluated by detecting cell viability, colony formation and apoptosis. The present study determined that SChLAP1 was upregulated in TNBC tissues and was associated with the long-distant lymph node metastasis of patients with TNBC. Knockdown of SChLAP1 significantly inhibited cell viability and colony formation, and triggered apoptosis of TNBC cells. Bioinformatics analysis suggested that SChLAP1 acted as a sponge of microRNA (miR)-524-5p and negatively modulated the expression of miR-524-5p. An inverse correlation was also identified between the expression levels of SChLAP1 and miR-524-5p in TNBC tissues. Furthermore, the results demonstrated that SChLAP1 interacted with miR-524-5p, and subsequently regulated the expression level of High Mobility Group AT-Hook 2 (HMGA2) in TNBC cells. It was also found that the overexpression of HMGA2 rescued the suppressed viability of TNBC cells induced by SChLAP1 knockdown. In conclusion, the present findings demonstrated that SChLAP1 modulated the malignant tumor behaviors of TNBC cells by regulating HMGA2 and subsequently restraining miR-524-5p. D.A. Spandidos 2021-06 2021-04-12 /pmc/articles/PMC8060801/ /pubmed/33846810 http://dx.doi.org/10.3892/mmr.2021.12085 Text en Copyright: © Bai et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Bai, Xiangdong
Zhang, Shengxiao
Qiao, Jun
Xing, Xiaolong
Li, Weina
Zhang, Huanhu
Xie, Jun
Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis
title Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis
title_full Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis
title_fullStr Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis
title_full_unstemmed Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis
title_short Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis
title_sort long non-coding rna schlap1 regulates the proliferation of triple negative breast cancer cells via the mir-524-5p/hmga2 axis
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8060801/
https://www.ncbi.nlm.nih.gov/pubmed/33846810
http://dx.doi.org/10.3892/mmr.2021.12085
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