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LINC01116 Promotes Migration and Invasion of Oral Squamous Cell Carcinoma by Acting as a Competed Endogenous RNA in Regulation of MMP1 Expression
Oral squamous cell carcinoma (OSCC) has increasingly become a worldwide health concern, and its survival rate has not been much improved partially due to a deficiency of precise molecular markers. Dysregulation of LINC01116, a long noncoding RNA sequence, has been observed in several types of cancer...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9232319/ https://www.ncbi.nlm.nih.gov/pubmed/35756415 http://dx.doi.org/10.1155/2022/2857022 |
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author | Ying, Yukang Liu, Dong Zhao, Yue Zhong, Yuan Xu, Xuhui Luo, Jun Zhang, Zhenxing |
author_facet | Ying, Yukang Liu, Dong Zhao, Yue Zhong, Yuan Xu, Xuhui Luo, Jun Zhang, Zhenxing |
author_sort | Ying, Yukang |
collection | PubMed |
description | Oral squamous cell carcinoma (OSCC) has increasingly become a worldwide health concern, and its survival rate has not been much improved partially due to a deficiency of precise molecular markers. Dysregulation of LINC01116, a long noncoding RNA sequence, has been observed in several types of cancer. However, the role played by LINC01116 in OSCC has not yet been fully elaborated. This study explored how LINC01116 was involved in the regulation of OSCC progression by analyzing expressions of LINC01116 in OSCC patients. The findings demonstrated upregulation of LINC01116 in OSCC tissues as opposed to regular oral mucosa, and overexpression of LINC01116 was correlated with advanced tumor status. LINC01116 knockdown using shRNA markedly reduced the OSCC cell invasion and migration in vitro. Moreover, the expression of LINC01116 was negatively correlated with that of microRNA-9-5p (miR-9). Luciferase reporter and loss-of-function assays demonstrated that LINC01116 functioned as a competing endogenous RNA (ceRNA) that could effectively sponge miR-9, thus regulating the derepression of matrix metalloproteinase 1 (MMP1). Furthermore, we confirmed that LINC01116 knockdown did not affect the expression of MMP1 messenger RNA (mRNA). Collectively, it is demonstrated in this study that overexpression of LINC01116 can promote the OSCC progression. The LINC01116–miR-9-MMP1 axis provides a novel insight into the OSCC pathogenesis and offers potential therapeutic targets against OSCC. |
format | Online Article Text |
id | pubmed-9232319 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-92323192022-06-25 LINC01116 Promotes Migration and Invasion of Oral Squamous Cell Carcinoma by Acting as a Competed Endogenous RNA in Regulation of MMP1 Expression Ying, Yukang Liu, Dong Zhao, Yue Zhong, Yuan Xu, Xuhui Luo, Jun Zhang, Zhenxing Comput Math Methods Med Research Article Oral squamous cell carcinoma (OSCC) has increasingly become a worldwide health concern, and its survival rate has not been much improved partially due to a deficiency of precise molecular markers. Dysregulation of LINC01116, a long noncoding RNA sequence, has been observed in several types of cancer. However, the role played by LINC01116 in OSCC has not yet been fully elaborated. This study explored how LINC01116 was involved in the regulation of OSCC progression by analyzing expressions of LINC01116 in OSCC patients. The findings demonstrated upregulation of LINC01116 in OSCC tissues as opposed to regular oral mucosa, and overexpression of LINC01116 was correlated with advanced tumor status. LINC01116 knockdown using shRNA markedly reduced the OSCC cell invasion and migration in vitro. Moreover, the expression of LINC01116 was negatively correlated with that of microRNA-9-5p (miR-9). Luciferase reporter and loss-of-function assays demonstrated that LINC01116 functioned as a competing endogenous RNA (ceRNA) that could effectively sponge miR-9, thus regulating the derepression of matrix metalloproteinase 1 (MMP1). Furthermore, we confirmed that LINC01116 knockdown did not affect the expression of MMP1 messenger RNA (mRNA). Collectively, it is demonstrated in this study that overexpression of LINC01116 can promote the OSCC progression. The LINC01116–miR-9-MMP1 axis provides a novel insight into the OSCC pathogenesis and offers potential therapeutic targets against OSCC. Hindawi 2022-06-17 /pmc/articles/PMC9232319/ /pubmed/35756415 http://dx.doi.org/10.1155/2022/2857022 Text en Copyright © 2022 Yukang Ying et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Ying, Yukang Liu, Dong Zhao, Yue Zhong, Yuan Xu, Xuhui Luo, Jun Zhang, Zhenxing LINC01116 Promotes Migration and Invasion of Oral Squamous Cell Carcinoma by Acting as a Competed Endogenous RNA in Regulation of MMP1 Expression |
title | LINC01116 Promotes Migration and Invasion of Oral Squamous Cell Carcinoma by Acting as a Competed Endogenous RNA in Regulation of MMP1 Expression |
title_full | LINC01116 Promotes Migration and Invasion of Oral Squamous Cell Carcinoma by Acting as a Competed Endogenous RNA in Regulation of MMP1 Expression |
title_fullStr | LINC01116 Promotes Migration and Invasion of Oral Squamous Cell Carcinoma by Acting as a Competed Endogenous RNA in Regulation of MMP1 Expression |
title_full_unstemmed | LINC01116 Promotes Migration and Invasion of Oral Squamous Cell Carcinoma by Acting as a Competed Endogenous RNA in Regulation of MMP1 Expression |
title_short | LINC01116 Promotes Migration and Invasion of Oral Squamous Cell Carcinoma by Acting as a Competed Endogenous RNA in Regulation of MMP1 Expression |
title_sort | linc01116 promotes migration and invasion of oral squamous cell carcinoma by acting as a competed endogenous rna in regulation of mmp1 expression |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9232319/ https://www.ncbi.nlm.nih.gov/pubmed/35756415 http://dx.doi.org/10.1155/2022/2857022 |
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