Abstract A51: Nicotine induces cervical lymph node metastasis of mouse tongue cancer by regulating Prx1 /EMT signaling
| Autor: | Min Wang, Xiaofei Tang, Wenwen Niu, Moci Qi |
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| Rok vydání: | 2018 |
| Předmět: | |
| Zdroj: | Cancer Research. 78:A51-A51 |
| ISSN: | 1538-7445 0008-5472 |
| DOI: | 10.1158/1538-7445.mousemodels17-a51 |
| Popis: | Oral squamous cell carcinoma (OSCC) represents one of the most common malignant neoplasms worldwide, while tobacco is a major risk factor for OSCC. Nicotine has been reported to induce EMT and promote the progression in several malignant tumors. Our previous study showed that upregulation of Peroxiredoxin 1(PRX1) expression was observed and associated with nicotine-induced oxidative stress in OSCC. However, the effects of nicotine and the underlying molecular mechanisms on the development of OSCC metastases are not completely understood. Here, we established the cervical metastasis mouse models of tongue cancer by orthotopic transplantation of OSCC cell line siControl CAL 27 cells and siPRX1 CAL 27 cells labeled with GFP into the tongues of nude mice, in order to investigate the roles and mechanisms of nicotine in OSCC metastasis. Fluorescence stereomicroscopy was used to confirm the tumor formation and the development of cervical metastases, which the tumor cells showed distinct green fluorescence in mouse tongues and lymph nodes. The results showed that at day 13 after CAL 27 cell implantation, nicotine promoted OSCC growth in the tongues and metastatic rates of cervical lymph node in mice compared with control. Histologic examination and immunohistochemical staining with anti-keratin antibody further confirmed tumor formation and lymph node metastases. Nicotine treatment was shown to promote the downregulation of expression levels of E-cadherin, and upregulation of vimentin and Snail expression in tongues and lymph nodes, compared with those in the control mice. PRX1 knockdown led to the reduction in the metastasis rate, upregulation of E-cadherin expression, and downregulation of vimentin and Snail expression in tongues and lymph nodes. No significant differences were seen in the cervical lymph node metastatic rates and the expression of EMT-related markers between nicotine-treated and vehicle-treated mice after PRX1 knockdown. These results suggest that nicotine may induce cervical lymph node metastases through the regulation of Prx1/EMT signal pathway during OSCC pathogenesis. PRX1 plays a critical role in nicotine-induced metastasis of OSCC. Citation Format: Min Wang, Wenwen Niu, Moci Qi, Xiaofei Tang. Nicotine induces cervical lymph node metastasis of mouse tongue cancer by regulating Prx1 /EMT signaling [abstract]. In: Proceedings of the AACR Special Conference: Advances in Modeling Cancer in Mice: Technology, Biology, and Beyond; 2017 Sep 24-27; Orlando, Florida. Philadelphia (PA): AACR; Cancer Res 2018;78(10 Suppl):Abstract nr A51. |
| Databáze: | OpenAIRE |
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