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尼古丁暴露通过Snail-RKIP信号通路对头颈部鳞状细胞癌肿瘤进展的调控

Regulation of tumor progression via the Snail-RKIP signaling pathway by nicotine exposure in head and neck squamous cell carcinoma.

作者信息

Nieh Shin, Jao Shu-Wen, Yang Chin-Yuh, Lin Yaoh-Shiang, Tseng Yi-Han, Liu Chia-Lin, Lee Tsai-Yu, Liu Tsung-Yun, Chu Yueng-Hsiang, Chen Su-Feng

机构信息

Department and Graduate School of Pathology, National Defense Medical Center & Tri-Service General Hospital, Taipei, Taiwan.

Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.

出版信息

Head Neck. 2015 Dec;37(12):1712-21. doi: 10.1002/hed.23820. Epub 2015 Jun 18.

DOI:10.1002/hed.23820
PMID:24986226
Abstract

BACKGROUND: Recent studies suggest that long-term exposure of the carcinogen 4-methylnitrosamino-1-3-pyridyl-1-butanone (NNK) found in tobacco smoke is involved in the progression of head and neck squamous cell carcinoma (HNSCC). The underlying nicotine-mediated mechanism remains unclear. METHODS: An analysis of SCC-25 and Fadu cells with or without NNK exposure focusing on the evaluation of migration and invasion abilities, the expression of epithelial-mesenchymal transition, drug-resistance-related genes, properties of cancer stem cells (CSCs), and anti-apoptosis was performed. RESULTS: Long-term NNK exposure enhances migration and invasion with morphological alterations in a dose-dependently manner. Furthermore, NNK exposure also upregulates Snail, promotes sphere-forming ability, and overexpresses aldehyde dehydrogenase 1 (ALDH1), Nanog, OCT4, ABCG2, and MDR1. CONCLUSION: The current study confirmed that long-term NNK exposure plays a role in HNSCC by increasing anti-apoptosis and therapeutic resistance via the Snail-RKIP signaling pathway. Our data also suggest that α7 nicotinic acetylcholine receptor (α7-nAChR) inhibition or targeting Snail may provide a feasible rationale for preventing the progression of HNSCC.

摘要

背景：近期研究表明，烟草烟雾中发现的致癌物4-甲基亚硝胺基-1-(3-吡啶基)-1-丁酮（NNK）的长期暴露与头颈部鳞状细胞癌（HNSCC）的进展有关。潜在的尼古丁介导机制仍不清楚。 方法：对暴露或未暴露于NNK的SCC-25和Fadu细胞进行分析，重点评估迁移和侵袭能力、上皮-间质转化的表达、耐药相关基因、癌症干细胞（CSC）特性以及抗凋亡情况。 结果：长期NNK暴露以剂量依赖方式增强迁移和侵袭并伴有形态改变。此外，NNK暴露还上调Snail、促进成球能力，并使醛脱氢酶1（ALDH1）、Nanog、OOOorkun，促进成球能力，并使醛脱氢酶1（ALDH1）、Nanog、OCT4、ABCG2和MDR1过表达。 结论：当前研究证实，长期NNK暴露通过Snail-RKIP信号通路增加抗凋亡和治疗耐药性，在HNSCC中发挥作用。我们的数据还表明，抑制α7烟碱型乙酰胆碱受体（α7-nAChR）或靶向Snail可能为预防HNSCC进展提供可行的理论依据。 （原文中“orkun”疑似有误，未进行翻译调整）

相似文献

[1]
Regulation of tumor progression via the Snail-RKIP signaling pathway by nicotine exposure in head and neck squamous cell carcinoma.

Head Neck. 2015-12

[2]
Increased chemoresistance via Snail-Raf kinase inhibitor protein signaling in colorectal cancer in response to a nicotine derivative.

Oncotarget. 2016-4-26

[3]
Tobacco-specific carcinogen enhances colon cancer cell migration through alpha7-nicotinic acetylcholine receptor.

Ann Surg. 2009-6

[4]
Exposure to nicotine-derived nitrosamine ketone and arecoline synergistically facilitates tumor aggressiveness via overexpression of epidermal growth factor receptor and its downstream signaling in head and neck squamous cell carcinoma.

PLoS One. 2018-8-27

[5]
Enhancement of cancer stem-like and epithelial-mesenchymal transdifferentiation property in oral epithelial cells with long-term nicotine exposure: reversal by targeting SNAIL.

Toxicol Appl Pharmacol. 2012-12-3

[6]
CD44(high) /ALDH1(high) head and neck squamous cell carcinoma cells exhibit mesenchymal characteristics and GSK3β-dependent cancer stem cell properties.

J Oral Pathol Med. 2016-3

[7]
NNK enhances cell migration through α7-nicotinic acetylcholine receptor accompanied by increased of fibronectin expression in gastric cancer.

Ann Surg Oncol. 2011-10-4

[8]
Snail-induced EMT promotes cancer stem cell-like properties in head and neck cancer cells.

Oncol Rep. 2016-1

[9]
Acquisition cancer stemness, mesenchymal transdifferentiation, and chemoresistance properties by chronic exposure of oral epithelial cells to arecoline.

Oncotarget. 2016-12-20

[10]
Snail-induced epithelial-mesenchymal transition promotes cancer stem cell-like phenotype in head and neck cancer cells.

Int J Oncol. 2013-12-23

引用本文的文献

[1]
ABCG2, CD44 and SOX9 are increased with the acquisition of drug resistance and involved in cancer stem cell activities in head and neck squamous cell carcinoma cells.

Exp Ther Med. 2022-10-18

[2]
Expression, correlation, and prognostic significance of different nicotinic acetylcholine receptors, programed death ligand 1, and dopamine receptor D2 in lung adenocarcinoma.

Front Oncol. 2022-8-22

[3]
Elevated LSD1 and SNAIL Expression Indicate Poor Prognosis in Hypopharynx Carcinoma.

Int J Mol Sci. 2022-5-3

[4]
α-Conotoxins and α-Cobratoxin Promote, while Lipoxygenase and Cyclooxygenase Inhibitors Suppress the Proliferation of Glioma C6 Cells.

Mar Drugs. 2021-2-21

[5]
Effects of Genetic Polymorphisms of Drug Transporter ABCB1 (MDR1) and Cytochrome P450 Enzymes CYP2A6, CYP2B6 on Nicotine Addiction and Smoking Cessation.

Front Genet. 2020-11-30

[6]
Ion Channel Dysregulation in Head and Neck Cancers: Perspectives for Clinical Application.

Rev Physiol Biochem Pharmacol. 2021

[7]
An Integrated Genomic Strategy to Identify CHRNB4 as a Diagnostic/Prognostic Biomarker for Targeted Therapy in Head and Neck Cancer.

Cancers (Basel). 2020-5-22

[8]
miR-181a Upregulation Promotes Radioresistance of Nasopharyngeal Carcinoma by Targeting RKIP.

Onco Targets Ther. 2019-12-11

[9]
Cervical Cancer Correlates with the Differential Expression of Nicotinic Acetylcholine Receptors and Reveals Therapeutic Targets.

Mar Drugs. 2019-4-28

[10]
Exposure to nicotine-derived nitrosamine ketone and arecoline synergistically facilitates tumor aggressiveness via overexpression of epidermal growth factor receptor and its downstream signaling in head and neck squamous cell carcinoma.

PLoS One. 2018-8-27

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