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Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1

BACKGROUND: Colorectal cancer (CRC) is one of most common cancers worldwide. Long non-coding RNA SNHG6 has been reported to act as essential regulators in several cancers. However, the functional role and molecular mechanism of SNHG6 in colorectal cancer remain unclear. METHODS: Quantitative real-ti...

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Autores principales: Zhu, Yuekun, Xing, Yanwei, Chi, Fengxu, Sun, Weidong, Zhang, Zhiyong, Piao, Daxun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6140718/
https://www.ncbi.nlm.nih.gov/pubmed/30254467
http://dx.doi.org/10.2147/OTT.S170246
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author Zhu, Yuekun
Xing, Yanwei
Chi, Fengxu
Sun, Weidong
Zhang, Zhiyong
Piao, Daxun
author_facet Zhu, Yuekun
Xing, Yanwei
Chi, Fengxu
Sun, Weidong
Zhang, Zhiyong
Piao, Daxun
author_sort Zhu, Yuekun
collection PubMed
description BACKGROUND: Colorectal cancer (CRC) is one of most common cancers worldwide. Long non-coding RNA SNHG6 has been reported to act as essential regulators in several cancers. However, the functional role and molecular mechanism of SNHG6 in colorectal cancer remain unclear. METHODS: Quantitative real-time polymerase chain reaction (PCR) was performed to evaluate the SNHG6 expression in CRC tissues. Colony formation, transwell assays and in vivo mice models were carried out to assess the effect of SNHG6 on CRC biological functions. RESULTS: In the present study, we showed that the expression of SNHG6 was significantly upregulated in CRC tissues and cell lines. High expression of SNHG6 was associated with shorter overall survival in CRC patients. Functionally, SNHG6 knockdown significantly inhibited cell proliferation, invasion and migration both in vitro and in vivo. Mechanically, miR-760 was a direct target of SNHG6, and repression of miR-760 could rescue the inhibitory effect of SNHG6 knockdown on CRC progression. In addition, SNHG6 positively regulated FOXC1 expression through sponging miR-760 in CRC cells, thus indicating that SNHG6 exerted an oncogenic role in CRC by acting as a ceRNA of miR-760. CONCLUSION: Our results indicate that long non-coding RNA SNHG6 promotes colorectal cancer progression by sequestering miR-760 and activating FOXC1, our findings suggest that SNHG6 may serve as a potential therapeutic target for CRC.
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spelling pubmed-61407182018-09-25 Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1 Zhu, Yuekun Xing, Yanwei Chi, Fengxu Sun, Weidong Zhang, Zhiyong Piao, Daxun Onco Targets Ther Original Research BACKGROUND: Colorectal cancer (CRC) is one of most common cancers worldwide. Long non-coding RNA SNHG6 has been reported to act as essential regulators in several cancers. However, the functional role and molecular mechanism of SNHG6 in colorectal cancer remain unclear. METHODS: Quantitative real-time polymerase chain reaction (PCR) was performed to evaluate the SNHG6 expression in CRC tissues. Colony formation, transwell assays and in vivo mice models were carried out to assess the effect of SNHG6 on CRC biological functions. RESULTS: In the present study, we showed that the expression of SNHG6 was significantly upregulated in CRC tissues and cell lines. High expression of SNHG6 was associated with shorter overall survival in CRC patients. Functionally, SNHG6 knockdown significantly inhibited cell proliferation, invasion and migration both in vitro and in vivo. Mechanically, miR-760 was a direct target of SNHG6, and repression of miR-760 could rescue the inhibitory effect of SNHG6 knockdown on CRC progression. In addition, SNHG6 positively regulated FOXC1 expression through sponging miR-760 in CRC cells, thus indicating that SNHG6 exerted an oncogenic role in CRC by acting as a ceRNA of miR-760. CONCLUSION: Our results indicate that long non-coding RNA SNHG6 promotes colorectal cancer progression by sequestering miR-760 and activating FOXC1, our findings suggest that SNHG6 may serve as a potential therapeutic target for CRC. Dove Medical Press 2018-09-12 /pmc/articles/PMC6140718/ /pubmed/30254467 http://dx.doi.org/10.2147/OTT.S170246 Text en © 2018 Zhu et al. 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.
spellingShingle Original Research
Zhu, Yuekun
Xing, Yanwei
Chi, Fengxu
Sun, Weidong
Zhang, Zhiyong
Piao, Daxun
Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1
title Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1
title_full Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1
title_fullStr Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1
title_full_unstemmed Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1
title_short Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1
title_sort long noncoding rna snhg6 promotes the progression of colorectal cancer through sponging mir-760 and activation of foxc1
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6140718/
https://www.ncbi.nlm.nih.gov/pubmed/30254467
http://dx.doi.org/10.2147/OTT.S170246
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