Aspirin is Involved in the Cell Cycle Arrest, Apoptosis, Cell Migration, and Invasion of Oral Squamous Cell Carcinoma
Oral squamous cell carcinoma (OSCC) is one of the most common cancers worldwide. In China, its 5-year survival rate is roughly 50%, owing to acquired chemotherapeutic resistance and metastasis of the disease. Accumulating evidence demonstrates that aspirin (ASA) acts as a preventive or therapeutic a...
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MDPI AG
2018-07-01
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author | Xiaoqi Zhang Hao Feng Ziyu Li Jie Guo Minqi Li |
author_facet | Xiaoqi Zhang Hao Feng Ziyu Li Jie Guo Minqi Li |
author_sort | Xiaoqi Zhang |
collection | DOAJ |
description | Oral squamous cell carcinoma (OSCC) is one of the most common cancers worldwide. In China, its 5-year survival rate is roughly 50%, owing to acquired chemotherapeutic resistance and metastasis of the disease. Accumulating evidence demonstrates that aspirin (ASA) acts as a preventive or therapeutic agent in multiple cancers; however, anti-tumor activities induced by aspirin are unclear in OSCC. To investigate the possible role of aspirin in OSCC development, we first employed bioinformatics to analyze the anti-OSCC effects of aspirin. We performed a genetic oncology (GO) enrichment analysis using the Database for Annotation, Visualization, and Integrated Discovery (DAVID), and the protein–protein interaction (PPI) network analysis by Cytoscape for differentially expressed genes (DEGs). We also evaluated the potential effects of aspirin on cell proliferation, invasion, migration, and apoptosis in two well-characterized OSCC cell lines (TCA8113 and CAL27). The bioinformatic results revealed that aspirin could inhibit proliferation by blocking the cell cycle, and could reduce migration and invasion via the PI3K-Akt and focal adhesion pathways. We found that ASA could downregulate the OSCC cell proliferation colony formation, invasion, and migration, as well as upregulate apoptosis. Furthermore, we found that ASA suppressed the activation of the focal adhesion kinase (FAK) and the phosphorylation of Akt, NF-κB, and STAT3. Overall, our data suggested that ASA may be developed as a chemopreventive agent to effectively treat OSCC. |
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spelling | doaj.art-f2e0d0b521e74922b957d0cabb0364ee2022-12-22T02:47:27ZengMDPI AGInternational Journal of Molecular Sciences1422-00672018-07-01197202910.3390/ijms19072029ijms19072029Aspirin is Involved in the Cell Cycle Arrest, Apoptosis, Cell Migration, and Invasion of Oral Squamous Cell CarcinomaXiaoqi Zhang0Hao Feng1Ziyu Li2Jie Guo3Minqi Li4Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Department of Bone Metabolism, School of Stomatology Shandong University, Jinan 250012, ChinaShandong Provincial Key Laboratory of Oral Tissue Regeneration, Department of Bone Metabolism, School of Stomatology Shandong University, Jinan 250012, ChinaShandong Provincial Key Laboratory of Oral Tissue Regeneration, Department of Bone Metabolism, School of Stomatology Shandong University, Jinan 250012, ChinaShandong Provincial Key Laboratory of Oral Tissue Regeneration, Department of Orthodontics, School of Stomatology Shandong University, Jinan 250012, ChinaShandong Provincial Key Laboratory of Oral Tissue Regeneration, Department of Bone Metabolism, School of Stomatology Shandong University, Jinan 250012, ChinaOral squamous cell carcinoma (OSCC) is one of the most common cancers worldwide. In China, its 5-year survival rate is roughly 50%, owing to acquired chemotherapeutic resistance and metastasis of the disease. Accumulating evidence demonstrates that aspirin (ASA) acts as a preventive or therapeutic agent in multiple cancers; however, anti-tumor activities induced by aspirin are unclear in OSCC. To investigate the possible role of aspirin in OSCC development, we first employed bioinformatics to analyze the anti-OSCC effects of aspirin. We performed a genetic oncology (GO) enrichment analysis using the Database for Annotation, Visualization, and Integrated Discovery (DAVID), and the protein–protein interaction (PPI) network analysis by Cytoscape for differentially expressed genes (DEGs). We also evaluated the potential effects of aspirin on cell proliferation, invasion, migration, and apoptosis in two well-characterized OSCC cell lines (TCA8113 and CAL27). The bioinformatic results revealed that aspirin could inhibit proliferation by blocking the cell cycle, and could reduce migration and invasion via the PI3K-Akt and focal adhesion pathways. We found that ASA could downregulate the OSCC cell proliferation colony formation, invasion, and migration, as well as upregulate apoptosis. Furthermore, we found that ASA suppressed the activation of the focal adhesion kinase (FAK) and the phosphorylation of Akt, NF-κB, and STAT3. Overall, our data suggested that ASA may be developed as a chemopreventive agent to effectively treat OSCC.http://www.mdpi.com/1422-0067/19/7/2029oral squamous cell carcinomacell cycleinvasionmigrationapoptosisbioinformatics |
spellingShingle | Xiaoqi Zhang Hao Feng Ziyu Li Jie Guo Minqi Li Aspirin is Involved in the Cell Cycle Arrest, Apoptosis, Cell Migration, and Invasion of Oral Squamous Cell Carcinoma International Journal of Molecular Sciences oral squamous cell carcinoma cell cycle invasion migration apoptosis bioinformatics |
title | Aspirin is Involved in the Cell Cycle Arrest, Apoptosis, Cell Migration, and Invasion of Oral Squamous Cell Carcinoma |
title_full | Aspirin is Involved in the Cell Cycle Arrest, Apoptosis, Cell Migration, and Invasion of Oral Squamous Cell Carcinoma |
title_fullStr | Aspirin is Involved in the Cell Cycle Arrest, Apoptosis, Cell Migration, and Invasion of Oral Squamous Cell Carcinoma |
title_full_unstemmed | Aspirin is Involved in the Cell Cycle Arrest, Apoptosis, Cell Migration, and Invasion of Oral Squamous Cell Carcinoma |
title_short | Aspirin is Involved in the Cell Cycle Arrest, Apoptosis, Cell Migration, and Invasion of Oral Squamous Cell Carcinoma |
title_sort | aspirin is involved in the cell cycle arrest apoptosis cell migration and invasion of oral squamous cell carcinoma |
topic | oral squamous cell carcinoma cell cycle invasion migration apoptosis bioinformatics |
url | http://www.mdpi.com/1422-0067/19/7/2029 |
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