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Hsa_circ_0005379 regulates malignant behavior of oral squamous cell carcinoma through the EGFR pathway

BACKGROUND: Oral squamous cell carcinoma (OSCC) is an oral and maxillofacial malignancy with a high incidence worldwide. Accumulating evidence indicates that circular RNAs (circRNAs) play a vital role in modulating tumor development. However, the mechanism of circRNA action in human OSCC remains lar...

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Autores principales: Su, Wen, Wang, Yufan, Wang, Feng, Sun, Shuai, Li, Minghua, Shen, Yuehong, Yang, Hongyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6489207/
https://www.ncbi.nlm.nih.gov/pubmed/31035951
http://dx.doi.org/10.1186/s12885-019-5593-5
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author Su, Wen
Wang, Yufan
Wang, Feng
Sun, Shuai
Li, Minghua
Shen, Yuehong
Yang, Hongyu
author_facet Su, Wen
Wang, Yufan
Wang, Feng
Sun, Shuai
Li, Minghua
Shen, Yuehong
Yang, Hongyu
author_sort Su, Wen
collection PubMed
description BACKGROUND: Oral squamous cell carcinoma (OSCC) is an oral and maxillofacial malignancy with a high incidence worldwide. Accumulating evidence indicates that circular RNAs (circRNAs) play a vital role in modulating tumor development. However, the mechanism of circRNA action in human OSCC remains largely unknown. METHODS: By using high-throughput transcriptome sequencing technology, we conducted a comprehensive study of circRNAs in human OSCC. The effect of circRNA hsa_circ_0005379 on OSCC tissues and cell lines was monitored by qRT-PCR, Transwell assay, flow cytometry, and western blot analysis. Xenograft mouse models were used to assess tumor growth and animal survival. RESULTS: We found that circRNA hsa_circ_0005379 expression is significantly lower in OSCC tissue compared to paired non-cancerous matched tissue and is associated with tumor size and differentiation. Overexpression of hsa_circ_0005379 effectively inhibits migration, invasion, and proliferation of OSCC cells in vitro and suppresses OSCC growth in nude mice in vivo. Mechanistic studies revealed that hsa_circ_0005379 may be involved in the regulation of the epidermal growth factor receptor (EGFR) pathway. Furthermore, we found that high expression of hsa_circ_0005379 could significantly enhance the sensitivity of OSCC to the cetuximab drug. CONCLUSIONS: Our findings provide evidence that hsa_circ_0005379 regulates OSCC malignancy and may be a new therapeutic target for OSCC treatment. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12885-019-5593-5) contains supplementary material, which is available to authorized users.
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spelling pubmed-64892072019-06-05 Hsa_circ_0005379 regulates malignant behavior of oral squamous cell carcinoma through the EGFR pathway Su, Wen Wang, Yufan Wang, Feng Sun, Shuai Li, Minghua Shen, Yuehong Yang, Hongyu BMC Cancer Research Article BACKGROUND: Oral squamous cell carcinoma (OSCC) is an oral and maxillofacial malignancy with a high incidence worldwide. Accumulating evidence indicates that circular RNAs (circRNAs) play a vital role in modulating tumor development. However, the mechanism of circRNA action in human OSCC remains largely unknown. METHODS: By using high-throughput transcriptome sequencing technology, we conducted a comprehensive study of circRNAs in human OSCC. The effect of circRNA hsa_circ_0005379 on OSCC tissues and cell lines was monitored by qRT-PCR, Transwell assay, flow cytometry, and western blot analysis. Xenograft mouse models were used to assess tumor growth and animal survival. RESULTS: We found that circRNA hsa_circ_0005379 expression is significantly lower in OSCC tissue compared to paired non-cancerous matched tissue and is associated with tumor size and differentiation. Overexpression of hsa_circ_0005379 effectively inhibits migration, invasion, and proliferation of OSCC cells in vitro and suppresses OSCC growth in nude mice in vivo. Mechanistic studies revealed that hsa_circ_0005379 may be involved in the regulation of the epidermal growth factor receptor (EGFR) pathway. Furthermore, we found that high expression of hsa_circ_0005379 could significantly enhance the sensitivity of OSCC to the cetuximab drug. CONCLUSIONS: Our findings provide evidence that hsa_circ_0005379 regulates OSCC malignancy and may be a new therapeutic target for OSCC treatment. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12885-019-5593-5) contains supplementary material, which is available to authorized users. BioMed Central 2019-04-29 /pmc/articles/PMC6489207/ /pubmed/31035951 http://dx.doi.org/10.1186/s12885-019-5593-5 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Su, Wen
Wang, Yufan
Wang, Feng
Sun, Shuai
Li, Minghua
Shen, Yuehong
Yang, Hongyu
Hsa_circ_0005379 regulates malignant behavior of oral squamous cell carcinoma through the EGFR pathway
title Hsa_circ_0005379 regulates malignant behavior of oral squamous cell carcinoma through the EGFR pathway
title_full Hsa_circ_0005379 regulates malignant behavior of oral squamous cell carcinoma through the EGFR pathway
title_fullStr Hsa_circ_0005379 regulates malignant behavior of oral squamous cell carcinoma through the EGFR pathway
title_full_unstemmed Hsa_circ_0005379 regulates malignant behavior of oral squamous cell carcinoma through the EGFR pathway
title_short Hsa_circ_0005379 regulates malignant behavior of oral squamous cell carcinoma through the EGFR pathway
title_sort hsa_circ_0005379 regulates malignant behavior of oral squamous cell carcinoma through the egfr pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6489207/
https://www.ncbi.nlm.nih.gov/pubmed/31035951
http://dx.doi.org/10.1186/s12885-019-5593-5
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