Cigarette smoking induces the activation of RIP2/caspase-12/NF-κB axis in oral squamous cell carcinoma
Cigarette smoking is one of the major risk factors for the occurrence and progression of oral squamous cell carcinoma (OSCC). Receptor-interacting protein 2 (RIP2) has been involved in mucosal immunity and homeostasis via a positive regulation of nuclear factor κB (NF-κB) transcription factor activi...
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PeerJ Inc.
2022-11-01
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Online Access: | https://peerj.com/articles/14330.pdf |
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author | Yajie Qian Wenmei Wang Deyan Chen Yanan Zhu Yong Wang Xiang Wang |
author_facet | Yajie Qian Wenmei Wang Deyan Chen Yanan Zhu Yong Wang Xiang Wang |
author_sort | Yajie Qian |
collection | DOAJ |
description | Cigarette smoking is one of the major risk factors for the occurrence and progression of oral squamous cell carcinoma (OSCC). Receptor-interacting protein 2 (RIP2) has been involved in mucosal immunity and homeostasis via a positive regulation of nuclear factor κB (NF-κB) transcription factor activity. Caspase-12 can bind to RIP2 and dampen mucosal immunity. However, the roles of RIP2/NF-κB and caspase-12 in OSCC induced by cigarette smoking remain unknown. Herein, we investigated the effects of cigarette smoking on the RIP2/NF-κB and caspase-12 in human OSCC tissues and OSCC cell lines (HSC-3). We first observed that RIP2 mediated NF-κB activation and caspase-12 upregulation in OSCC patients with cigarette smoking and cigarette smoke extract (CSE)-treated HSC-3 cells, respectively. Moreover, we confirmed that the downregulation of RIP2 by siRNA resulted in the reduction of caspase-12 expression and NF-κB activity in the presence of CSE treatment in vitro. In summary, our results indicated that cigarette smoking induced the activation of the RIP2/caspase-12/NF-κB axis and it played an important role in the development of OSCC. The RIP2/caspase-12/NF-κB axis could be a target for OSCC prevention and treatment in the future. |
first_indexed | 2024-03-09T08:06:28Z |
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id | doaj.art-6ef42e59e92d4bdea337915568fca3a2 |
institution | Directory Open Access Journal |
issn | 2167-8359 |
language | English |
last_indexed | 2024-03-09T08:06:28Z |
publishDate | 2022-11-01 |
publisher | PeerJ Inc. |
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spelling | doaj.art-6ef42e59e92d4bdea337915568fca3a22023-12-02T23:47:59ZengPeerJ Inc.PeerJ2167-83592022-11-0110e1433010.7717/peerj.14330Cigarette smoking induces the activation of RIP2/caspase-12/NF-κB axis in oral squamous cell carcinomaYajie Qian0Wenmei Wang1Deyan Chen2Yanan Zhu3Yong Wang4Xiang Wang5Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, ChinaNanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, ChinaState Key Laboratory of Analytical Chemistry for Life Science & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, ChinaNanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, ChinaState Key Laboratory of Analytical Chemistry for Life Science & Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, ChinaNanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, ChinaCigarette smoking is one of the major risk factors for the occurrence and progression of oral squamous cell carcinoma (OSCC). Receptor-interacting protein 2 (RIP2) has been involved in mucosal immunity and homeostasis via a positive regulation of nuclear factor κB (NF-κB) transcription factor activity. Caspase-12 can bind to RIP2 and dampen mucosal immunity. However, the roles of RIP2/NF-κB and caspase-12 in OSCC induced by cigarette smoking remain unknown. Herein, we investigated the effects of cigarette smoking on the RIP2/NF-κB and caspase-12 in human OSCC tissues and OSCC cell lines (HSC-3). We first observed that RIP2 mediated NF-κB activation and caspase-12 upregulation in OSCC patients with cigarette smoking and cigarette smoke extract (CSE)-treated HSC-3 cells, respectively. Moreover, we confirmed that the downregulation of RIP2 by siRNA resulted in the reduction of caspase-12 expression and NF-κB activity in the presence of CSE treatment in vitro. In summary, our results indicated that cigarette smoking induced the activation of the RIP2/caspase-12/NF-κB axis and it played an important role in the development of OSCC. The RIP2/caspase-12/NF-κB axis could be a target for OSCC prevention and treatment in the future.https://peerj.com/articles/14330.pdfCigarette smokingOral squamous cell carcinomaRIP2Caspase-12NF-κB |
spellingShingle | Yajie Qian Wenmei Wang Deyan Chen Yanan Zhu Yong Wang Xiang Wang Cigarette smoking induces the activation of RIP2/caspase-12/NF-κB axis in oral squamous cell carcinoma PeerJ Cigarette smoking Oral squamous cell carcinoma RIP2 Caspase-12 NF-κB |
title | Cigarette smoking induces the activation of RIP2/caspase-12/NF-κB axis in oral squamous cell carcinoma |
title_full | Cigarette smoking induces the activation of RIP2/caspase-12/NF-κB axis in oral squamous cell carcinoma |
title_fullStr | Cigarette smoking induces the activation of RIP2/caspase-12/NF-κB axis in oral squamous cell carcinoma |
title_full_unstemmed | Cigarette smoking induces the activation of RIP2/caspase-12/NF-κB axis in oral squamous cell carcinoma |
title_short | Cigarette smoking induces the activation of RIP2/caspase-12/NF-κB axis in oral squamous cell carcinoma |
title_sort | cigarette smoking induces the activation of rip2 caspase 12 nf κb axis in oral squamous cell carcinoma |
topic | Cigarette smoking Oral squamous cell carcinoma RIP2 Caspase-12 NF-κB |
url | https://peerj.com/articles/14330.pdf |
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