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ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis
Long non-coding RNAs (lncRNAs) play important regulatory roles in the initiation and progression of various cancers. However, the biological roles and the potential mechanisms of lncRNAs in gastric cancers remain unclear. Here, we report that the expression of lncRNA SNHG22 (small nucleolar RNA host...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8523719/ https://www.ncbi.nlm.nih.gov/pubmed/34663788 http://dx.doi.org/10.1038/s41419-021-04228-z |
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author | Mao, Xiaqiong Ji, Tao Liu, Aiguo Weng, Yunqi |
author_facet | Mao, Xiaqiong Ji, Tao Liu, Aiguo Weng, Yunqi |
author_sort | Mao, Xiaqiong |
collection | PubMed |
description | Long non-coding RNAs (lncRNAs) play important regulatory roles in the initiation and progression of various cancers. However, the biological roles and the potential mechanisms of lncRNAs in gastric cancers remain unclear. Here, we report that the expression of lncRNA SNHG22 (small nucleolar RNA host gene 22) was significantly increased in GC (Gastric Cancer) tissues and cells, which confers poor prognosis of patients. Knockdown of SNHG22 inhibited the proliferation and invasion ability of GC cells. Moreover, we identified that the transcriptional factor, ELK4 (ETS transcription factor ELK4), could promote SNHG22 expression in GC cells. In addition, using RNA pull-down followed MS assay, we found that SNHG22 directly bound to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) to suppress the expression of tumor suppressor genes. At the same time, SNHG22 sponged miR-200c-3p to increase Notch1 (notch receptor 1) expression. Taken together, our findings demonstrated the role of SNHG22 on promoting proliferation and invasion of GC cells. And we revealed a new regulatory mechanism of SNHG22 in GC cells. SNHG22 is a promising lncRNA biomarker for diagnosis and prognosis and a potential target for GC treatment. |
format | Online Article Text |
id | pubmed-8523719 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-85237192021-11-04 ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis Mao, Xiaqiong Ji, Tao Liu, Aiguo Weng, Yunqi Cell Death Dis Article Long non-coding RNAs (lncRNAs) play important regulatory roles in the initiation and progression of various cancers. However, the biological roles and the potential mechanisms of lncRNAs in gastric cancers remain unclear. Here, we report that the expression of lncRNA SNHG22 (small nucleolar RNA host gene 22) was significantly increased in GC (Gastric Cancer) tissues and cells, which confers poor prognosis of patients. Knockdown of SNHG22 inhibited the proliferation and invasion ability of GC cells. Moreover, we identified that the transcriptional factor, ELK4 (ETS transcription factor ELK4), could promote SNHG22 expression in GC cells. In addition, using RNA pull-down followed MS assay, we found that SNHG22 directly bound to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) to suppress the expression of tumor suppressor genes. At the same time, SNHG22 sponged miR-200c-3p to increase Notch1 (notch receptor 1) expression. Taken together, our findings demonstrated the role of SNHG22 on promoting proliferation and invasion of GC cells. And we revealed a new regulatory mechanism of SNHG22 in GC cells. SNHG22 is a promising lncRNA biomarker for diagnosis and prognosis and a potential target for GC treatment. Nature Publishing Group UK 2021-10-18 /pmc/articles/PMC8523719/ /pubmed/34663788 http://dx.doi.org/10.1038/s41419-021-04228-z Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Mao, Xiaqiong Ji, Tao Liu, Aiguo Weng, Yunqi ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis |
title | ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis |
title_full | ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis |
title_fullStr | ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis |
title_full_unstemmed | ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis |
title_short | ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis |
title_sort | elk4-mediated lncrna snhg22 promotes gastric cancer progression through interacting with ezh2 and regulating mir-200c-3p/notch1 axis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8523719/ https://www.ncbi.nlm.nih.gov/pubmed/34663788 http://dx.doi.org/10.1038/s41419-021-04228-z |
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