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SP1-induced long non-coding RNA SNHG6 facilitates the carcinogenesis of chondrosarcoma through inhibiting KLF6 by recruiting EZH2

Small nucleolar RNA host gene 6 (SNHG6) is a newly discovered long non-coding RNA (lncRNA), while the regulatory mechanism of SNHG6 in chondrosarcoma is largely unknown. Here we found that SNHG6 expression was upregulated and showed positive correlation with the progression of chondrosarcoma. Functi...

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Autores principales: Pu, Fei-Fei, Shi, De-Yao, Chen, Ting, Liu, Yu-Xuan, Zhong, Bin-Long, Zhang, Zhi-Cai, Liu, Wei-Jian, Wu, Qiang, Wang, Bai-Chuan, Shao, Zeng-Wu, He, Tong-Chuan, Liu, Jian-Xiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7801621/
https://www.ncbi.nlm.nih.gov/pubmed/33431838
http://dx.doi.org/10.1038/s41419-020-03352-6
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author Pu, Fei-Fei
Shi, De-Yao
Chen, Ting
Liu, Yu-Xuan
Zhong, Bin-Long
Zhang, Zhi-Cai
Liu, Wei-Jian
Wu, Qiang
Wang, Bai-Chuan
Shao, Zeng-Wu
He, Tong-Chuan
Liu, Jian-Xiang
author_facet Pu, Fei-Fei
Shi, De-Yao
Chen, Ting
Liu, Yu-Xuan
Zhong, Bin-Long
Zhang, Zhi-Cai
Liu, Wei-Jian
Wu, Qiang
Wang, Bai-Chuan
Shao, Zeng-Wu
He, Tong-Chuan
Liu, Jian-Xiang
author_sort Pu, Fei-Fei
collection PubMed
description Small nucleolar RNA host gene 6 (SNHG6) is a newly discovered long non-coding RNA (lncRNA), while the regulatory mechanism of SNHG6 in chondrosarcoma is largely unknown. Here we found that SNHG6 expression was upregulated and showed positive correlation with the progression of chondrosarcoma. Functional assays demonstrated that SNHG6 was required for the proliferation, migration, and invasion of chondrosarcoma cells. Mechanistic study revealed that SNHG6 could recruit EZH2 and maintain high level of H3K27me3 to repress the transcription of tumor-suppressor genes, including KLF6. KLF6 was found to bind to the promoter region of SP1 and restrained its transcription, while SP1 could be recruited to the promoter region of SNHG6 and promoted its transcription to form a positive loop. In summary, this study reveals that SP1-induced SNHG6 forms a positive loop to facilitate the carcinogenesis of chondrosarcoma through the suppression of KLF6 by recruiting EZH2, which manifests the oncogenic function of SNHG6 in chondrosarcoma.
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spelling pubmed-78016212021-01-21 SP1-induced long non-coding RNA SNHG6 facilitates the carcinogenesis of chondrosarcoma through inhibiting KLF6 by recruiting EZH2 Pu, Fei-Fei Shi, De-Yao Chen, Ting Liu, Yu-Xuan Zhong, Bin-Long Zhang, Zhi-Cai Liu, Wei-Jian Wu, Qiang Wang, Bai-Chuan Shao, Zeng-Wu He, Tong-Chuan Liu, Jian-Xiang Cell Death Dis Article Small nucleolar RNA host gene 6 (SNHG6) is a newly discovered long non-coding RNA (lncRNA), while the regulatory mechanism of SNHG6 in chondrosarcoma is largely unknown. Here we found that SNHG6 expression was upregulated and showed positive correlation with the progression of chondrosarcoma. Functional assays demonstrated that SNHG6 was required for the proliferation, migration, and invasion of chondrosarcoma cells. Mechanistic study revealed that SNHG6 could recruit EZH2 and maintain high level of H3K27me3 to repress the transcription of tumor-suppressor genes, including KLF6. KLF6 was found to bind to the promoter region of SP1 and restrained its transcription, while SP1 could be recruited to the promoter region of SNHG6 and promoted its transcription to form a positive loop. In summary, this study reveals that SP1-induced SNHG6 forms a positive loop to facilitate the carcinogenesis of chondrosarcoma through the suppression of KLF6 by recruiting EZH2, which manifests the oncogenic function of SNHG6 in chondrosarcoma. Nature Publishing Group UK 2021-01-11 /pmc/articles/PMC7801621/ /pubmed/33431838 http://dx.doi.org/10.1038/s41419-020-03352-6 Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Pu, Fei-Fei
Shi, De-Yao
Chen, Ting
Liu, Yu-Xuan
Zhong, Bin-Long
Zhang, Zhi-Cai
Liu, Wei-Jian
Wu, Qiang
Wang, Bai-Chuan
Shao, Zeng-Wu
He, Tong-Chuan
Liu, Jian-Xiang
SP1-induced long non-coding RNA SNHG6 facilitates the carcinogenesis of chondrosarcoma through inhibiting KLF6 by recruiting EZH2
title SP1-induced long non-coding RNA SNHG6 facilitates the carcinogenesis of chondrosarcoma through inhibiting KLF6 by recruiting EZH2
title_full SP1-induced long non-coding RNA SNHG6 facilitates the carcinogenesis of chondrosarcoma through inhibiting KLF6 by recruiting EZH2
title_fullStr SP1-induced long non-coding RNA SNHG6 facilitates the carcinogenesis of chondrosarcoma through inhibiting KLF6 by recruiting EZH2
title_full_unstemmed SP1-induced long non-coding RNA SNHG6 facilitates the carcinogenesis of chondrosarcoma through inhibiting KLF6 by recruiting EZH2
title_short SP1-induced long non-coding RNA SNHG6 facilitates the carcinogenesis of chondrosarcoma through inhibiting KLF6 by recruiting EZH2
title_sort sp1-induced long non-coding rna snhg6 facilitates the carcinogenesis of chondrosarcoma through inhibiting klf6 by recruiting ezh2
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7801621/
https://www.ncbi.nlm.nih.gov/pubmed/33431838
http://dx.doi.org/10.1038/s41419-020-03352-6
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