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lncRNA DCST1-AS1 Facilitates Oral Squamous Cell Carcinoma by Promoting M2 Macrophage Polarization through Activating NF-κB Signaling
lncRNAs are related to the progression of various diseases, including oral squamous cell carcinoma (OSCC), which is a common squamous cell carcinoma of the head and neck. Tumor-associated macrophages and tumor cells are significant components of tumor microenvironment. M2 polarization of tumor-assoc...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369177/ https://www.ncbi.nlm.nih.gov/pubmed/34414241 http://dx.doi.org/10.1155/2021/5524231 |
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author | Ai, Yilong Liu, Shiwei Luo, Hailing Wu, Siyuan Wei, Haigang Tang, Zhe Li, Xia Zou, Chen |
author_facet | Ai, Yilong Liu, Shiwei Luo, Hailing Wu, Siyuan Wei, Haigang Tang, Zhe Li, Xia Zou, Chen |
author_sort | Ai, Yilong |
collection | PubMed |
description | lncRNAs are related to the progression of various diseases, including oral squamous cell carcinoma (OSCC), which is a common squamous cell carcinoma of the head and neck. Tumor-associated macrophages and tumor cells are significant components of tumor microenvironment. M2 polarization of tumor-associated macrophages is a crucial actor in tumor malignancy and metastasis. In this study, we studied the molecular mechanism of lncRNA DCST1-AS1 in OSCC. Here, we reported that DCST1-AS1 was significantly increased in OSCC cells. We found that loss of DCST1-AS1 obviously inhibited the proliferation, migration, and invasion of OSCC cells and xenograft tumor growth. Meanwhile, silencing of DCST1-AS1 also repressed the percentage of macrophages expressing M2 markers CD206 and CD11b. DCST1-AS1 shRNA enhanced the percentage of macrophages expressing M1 markers CD80 and CD11c. Then, we observed that loss of DCST1-AS1 suppressed OSCC progression via inactivating NF-κB signaling. As well established, NF-κB signaling exerts critical roles in tumor progression, and our study proved that DCST1-AS1 could regulate NF-κB signaling. We proved that blocking the NF-κB pathway using antagonists greatly downregulated OSCC progression and M2 macrophage polarization induced by the overexpression of DCST1-AS1. To sum up, we reported that DCST1-AS1 plays an important role in modulating OSCC tumorigenicity and M2 macrophage polarization through regulating the NF-κB pathway. |
format | Online Article Text |
id | pubmed-8369177 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-83691772021-08-18 lncRNA DCST1-AS1 Facilitates Oral Squamous Cell Carcinoma by Promoting M2 Macrophage Polarization through Activating NF-κB Signaling Ai, Yilong Liu, Shiwei Luo, Hailing Wu, Siyuan Wei, Haigang Tang, Zhe Li, Xia Zou, Chen J Immunol Res Research Article lncRNAs are related to the progression of various diseases, including oral squamous cell carcinoma (OSCC), which is a common squamous cell carcinoma of the head and neck. Tumor-associated macrophages and tumor cells are significant components of tumor microenvironment. M2 polarization of tumor-associated macrophages is a crucial actor in tumor malignancy and metastasis. In this study, we studied the molecular mechanism of lncRNA DCST1-AS1 in OSCC. Here, we reported that DCST1-AS1 was significantly increased in OSCC cells. We found that loss of DCST1-AS1 obviously inhibited the proliferation, migration, and invasion of OSCC cells and xenograft tumor growth. Meanwhile, silencing of DCST1-AS1 also repressed the percentage of macrophages expressing M2 markers CD206 and CD11b. DCST1-AS1 shRNA enhanced the percentage of macrophages expressing M1 markers CD80 and CD11c. Then, we observed that loss of DCST1-AS1 suppressed OSCC progression via inactivating NF-κB signaling. As well established, NF-κB signaling exerts critical roles in tumor progression, and our study proved that DCST1-AS1 could regulate NF-κB signaling. We proved that blocking the NF-κB pathway using antagonists greatly downregulated OSCC progression and M2 macrophage polarization induced by the overexpression of DCST1-AS1. To sum up, we reported that DCST1-AS1 plays an important role in modulating OSCC tumorigenicity and M2 macrophage polarization through regulating the NF-κB pathway. Hindawi 2021-08-08 /pmc/articles/PMC8369177/ /pubmed/34414241 http://dx.doi.org/10.1155/2021/5524231 Text en Copyright © 2021 Yilong Ai 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 Ai, Yilong Liu, Shiwei Luo, Hailing Wu, Siyuan Wei, Haigang Tang, Zhe Li, Xia Zou, Chen lncRNA DCST1-AS1 Facilitates Oral Squamous Cell Carcinoma by Promoting M2 Macrophage Polarization through Activating NF-κB Signaling |
title | lncRNA DCST1-AS1 Facilitates Oral Squamous Cell Carcinoma by Promoting M2 Macrophage Polarization through Activating NF-κB Signaling |
title_full | lncRNA DCST1-AS1 Facilitates Oral Squamous Cell Carcinoma by Promoting M2 Macrophage Polarization through Activating NF-κB Signaling |
title_fullStr | lncRNA DCST1-AS1 Facilitates Oral Squamous Cell Carcinoma by Promoting M2 Macrophage Polarization through Activating NF-κB Signaling |
title_full_unstemmed | lncRNA DCST1-AS1 Facilitates Oral Squamous Cell Carcinoma by Promoting M2 Macrophage Polarization through Activating NF-κB Signaling |
title_short | lncRNA DCST1-AS1 Facilitates Oral Squamous Cell Carcinoma by Promoting M2 Macrophage Polarization through Activating NF-κB Signaling |
title_sort | lncrna dcst1-as1 facilitates oral squamous cell carcinoma by promoting m2 macrophage polarization through activating nf-κb signaling |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369177/ https://www.ncbi.nlm.nih.gov/pubmed/34414241 http://dx.doi.org/10.1155/2021/5524231 |
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