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Toxicol Lett. 2018 Jul;291:70-76. doi: 10.1016/j.toxlet.2018.04.003. Epub 2018 Apr 4.

Wnt/β-catenin modulates chronic tobacco smoke exposure-induced acquisition of pulmonary cancer stem cell properties and diallyl trisulfide intervention.

Author information

1
School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
2
Department of Nutrition and Food Safety, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, China.
3
Department of Food and School Hygiene, Taizhou Municipal Center for Disease Control and Prevention, Taizhou, Zhejiang, 318000, China.
4
Suzhou Municipal Hospital, Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu, 215008, China.
5
Department of Nutrition and Food Safety, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, China; The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, China. Electronic address: cyzhong@njmu.edu.cn.
6
Department of Nutrition and Food Safety, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu, 211166, China. Electronic address: xiaotingli@njmu.edu.cn.

Abstract

Lung cancer is the leading cause of cancer-related death worldwide; tobacco smoke (TS) constitutes the main causes of lung cancer. Acquisition of cancer stem cells (CSCs)-like properties is the essential progression for the initiation of lung cancer. However, the mechanisms for tobacco smoke-induced lung carcinogenesis remain elusive. In the present study, we demonstrated that long-term exposure of human bronchial epithelial (HBE) cells to TS resulted in malignant transformation and acquisition of CSC-like properties. Moreover, Wnt/β-catenin pathway was involved in acquisition of the CSC-like phenotype during neoplastic transformation of HBE cells induced by TS. Downregulation of β-catenin reduced the tumorsphere and decreased the protein expression of lung CSCs markers in TS-transformated HBE sphere-forming cells. Furthermore, Diallyl trisulfide (DATS) inhibited the CSCs activity of TS-transformed HBE cells, as well as Wnt/β-catenin suppression. Activation of Wnt/β-catenin diminished the inhibitory effects of DATS on TS-induced stemness of HBE cells. Together, the present investigation elucidates the modulation of Wnt/β-catenin in chronic TS exposure-triggered pulmonary acquisition of CSCs properties and DATS intervention, which may provide new insights into the interventional strategies against lung CSCs.

KEYWORDS:

Cancer stem cells; DATS; Tobacco smoke; Wnt/β-catenin

PMID:
29626521
DOI:
10.1016/j.toxlet.2018.04.003
[Indexed for MEDLINE]

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