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LncRNA XIST Inhibits the Progression of Oral Squamous Cell Carcinoma via Sponging miR-455-3p/BTG2 Axis
OBJECTIVE: Oral squamous cell carcinoma (OSCC) is one of the most common cancers, accounting for over 90% of malignant lesions in the oral cavity. Long non-coding RNAs play an important role in the development of OSCC. This study aimed to investigate the effects of lncRNA XIST on the malignant behav...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7650041/ https://www.ncbi.nlm.nih.gov/pubmed/33177835 http://dx.doi.org/10.2147/OTT.S267937 |
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author | Li, Qingbin Sun, Qiang Zhu, Baoyu |
author_facet | Li, Qingbin Sun, Qiang Zhu, Baoyu |
author_sort | Li, Qingbin |
collection | PubMed |
description | OBJECTIVE: Oral squamous cell carcinoma (OSCC) is one of the most common cancers, accounting for over 90% of malignant lesions in the oral cavity. Long non-coding RNAs play an important role in the development of OSCC. This study aimed to investigate the effects of lncRNA XIST on the malignant behaviors of OSCC cells and its possible molecular mechanisms. METHODS: Real-time quantitative PCR and Western blot were used to detect the RNA and protein level, respectively. CAL27 and SCC25 cells with the lowest expression level of XIST were used for further study. MTT, transwell assay, colony formation, and xenograft model were applied to examine the effect of XIST on the progression of OSCC. FISH assay was performed to investigate the co-location of XIST and miR-455-3p in OSCC cells. The bioinformatics analysis, luciferase, and RNA pull down assay were utilized to predict and verify the target genes of miR-455-3p. RESULTS: XIST was downregulated in OSCC tissues and cell lines. Overexpression of XIST inhibited the proliferation, migration, and invasion ability of OSCC cells. Bioinformatics analysis and luciferase reporter assay confirmed XIST could bind to miR-455-3p. Besides, miR-455-3p directly targeted BTG2 in OSCC cells. Rescue experiments further confirmed the positive interaction between miR-455-3p and XIST as well as between miR-455-3p and BTG2. CONCLUSION: XIST was down-regulated in OSCC. XIST regulated the expression of BTG2 via sponging miR-455-3p. XIST/miR-455-3p/BTG2 signal axis inhibited the malignant progression of OSCC. |
format | Online Article Text |
id | pubmed-7650041 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-76500412020-11-10 LncRNA XIST Inhibits the Progression of Oral Squamous Cell Carcinoma via Sponging miR-455-3p/BTG2 Axis Li, Qingbin Sun, Qiang Zhu, Baoyu Onco Targets Ther Original Research OBJECTIVE: Oral squamous cell carcinoma (OSCC) is one of the most common cancers, accounting for over 90% of malignant lesions in the oral cavity. Long non-coding RNAs play an important role in the development of OSCC. This study aimed to investigate the effects of lncRNA XIST on the malignant behaviors of OSCC cells and its possible molecular mechanisms. METHODS: Real-time quantitative PCR and Western blot were used to detect the RNA and protein level, respectively. CAL27 and SCC25 cells with the lowest expression level of XIST were used for further study. MTT, transwell assay, colony formation, and xenograft model were applied to examine the effect of XIST on the progression of OSCC. FISH assay was performed to investigate the co-location of XIST and miR-455-3p in OSCC cells. The bioinformatics analysis, luciferase, and RNA pull down assay were utilized to predict and verify the target genes of miR-455-3p. RESULTS: XIST was downregulated in OSCC tissues and cell lines. Overexpression of XIST inhibited the proliferation, migration, and invasion ability of OSCC cells. Bioinformatics analysis and luciferase reporter assay confirmed XIST could bind to miR-455-3p. Besides, miR-455-3p directly targeted BTG2 in OSCC cells. Rescue experiments further confirmed the positive interaction between miR-455-3p and XIST as well as between miR-455-3p and BTG2. CONCLUSION: XIST was down-regulated in OSCC. XIST regulated the expression of BTG2 via sponging miR-455-3p. XIST/miR-455-3p/BTG2 signal axis inhibited the malignant progression of OSCC. Dove 2020-11-03 /pmc/articles/PMC7650041/ /pubmed/33177835 http://dx.doi.org/10.2147/OTT.S267937 Text en © 2020 Li et al. http://creativecommons.org/licenses/by-nc/3.0/ 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Li, Qingbin Sun, Qiang Zhu, Baoyu LncRNA XIST Inhibits the Progression of Oral Squamous Cell Carcinoma via Sponging miR-455-3p/BTG2 Axis |
title | LncRNA XIST Inhibits the Progression of Oral Squamous Cell Carcinoma via Sponging miR-455-3p/BTG2 Axis |
title_full | LncRNA XIST Inhibits the Progression of Oral Squamous Cell Carcinoma via Sponging miR-455-3p/BTG2 Axis |
title_fullStr | LncRNA XIST Inhibits the Progression of Oral Squamous Cell Carcinoma via Sponging miR-455-3p/BTG2 Axis |
title_full_unstemmed | LncRNA XIST Inhibits the Progression of Oral Squamous Cell Carcinoma via Sponging miR-455-3p/BTG2 Axis |
title_short | LncRNA XIST Inhibits the Progression of Oral Squamous Cell Carcinoma via Sponging miR-455-3p/BTG2 Axis |
title_sort | lncrna xist inhibits the progression of oral squamous cell carcinoma via sponging mir-455-3p/btg2 axis |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7650041/ https://www.ncbi.nlm.nih.gov/pubmed/33177835 http://dx.doi.org/10.2147/OTT.S267937 |
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