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

Wang, Jiaye; Chen, Jiaqi; Jiang, Ye; Shi, Yingying; Zhu, Jianyun; Xie, Chunfeng; Geng, Shanshan; Wu, Jieshu; Zhang, Qi; Wang, Xiaoqian; Meng, Yu; Li, Yuan; Chen, Yue; Cao, Wanshuang; Wang, Xueqi; Zhong, Caiyun; Li, Xiaoting

doi:10.1016/j.toxlet.2018.04.003

Cited by 25 publications

(18 citation statements)

References 44 publications

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“…Their findings suggest potential therapies for preventing or treating COPD using Wnt-signal modulators. The Wnt signal plays important roles in tissue homeostasis and cancer stem-cell proliferation and renewal in multiple organs, including lung (Wang et al, 2018). Therefore, the side effects should be considered during the development of therapeutic strategies to activate the Wnt pathway for COPD.…”

Section: Pharmacologically Targeting Wnt Signal Pathwaymentioning

confidence: 99%

Perspectives on Wnt Signal Pathway in the Pathogenesis and Therapeutics of Chronic Obstructive Pulmonary Disease

Gao

et al. 2019

J Pharmacol Exp Ther

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Chronic obstructive pulmonary disease (COPD) is a chronic lung disease with progressive airflow limitation and functional decline. The pathogenic mechanisms for this disease include oxidative stress, inflammatory responses, disturbed protease/antiprotease equilibrium, apoptosis/proliferation imbalance, senescence, autophagy, metabolic reprogramming, and mitochondrial dysfunction. The Wnt signaling pathway is an evolutionarily conserved signaling pathway that is abnormal in COPD, including chronic bronchitis and pulmonary emphysema. Furthermore, Wnt signaling has been shown to modulate aforementioned cellular processes involved in COPD. From this perspective, we provide an updated understanding of the crosstalk between Wnt signal and these cellular processes, and highlight the crucial role of the Wnt signal during the development of COPD. We also discuss the potential for targeting the Wnt signal in future translational and pharmacological therapeutics aimed at prevention and treatment of this disease.

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Section: Pharmacologically Targeting Wnt Signal Pathwaymentioning

confidence: 99%

Perspectives on Wnt Signal Pathway in the Pathogenesis and Therapeutics of Chronic Obstructive Pulmonary Disease

Gao

et al. 2019

J Pharmacol Exp Ther

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“…Cell layers were 70–80% confluent at the time of cigarette smoke extract (CSE) exposure. CSE was prepared daily immediately before use according to the reported method [28]. Briefly, one filterless 3R4F Research Reference Cigarette (University of Kentucky, 9 mg tar and 0.76 mg nicotine/cigarette) was combusted and the mainstream smoke was continuously drawn through a glass syringe containing 10 ml of fetal bovine serum free RPMI 1640 medium that was pre-warmed to 37 °C at a rate of 5 min/cigarette.…”

Section: Methodsmentioning

confidence: 99%

Tobacco smoke induced hepatic cancer stem cell-like properties through IL-33/p38 pathway

Xie

Zhu

Wang

et al. 2019

J Exp Clin Cancer Res

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BackgroundTobacco smoke (TS) critically contributes to the development of hepatocellular carcinoma. Cancer stem cells (CSCs) induced by TS is an early event in the initiation of carcinogenesis. Tumor specific microenvironment including inflammatory factors is key mediator for maintaining the stemness of CSCs through various pathways such as p38 MAPK. However, the mechanisms of inflammatory factors in TS-induced acquisition of liver CSCs properties remain undefined. The aim of this study was to investigate the role of IL-33/p38 axis in long term TS-induced acquisition of hepatic CSCs properties in mouse liver tissues and human liver cells.MethodsBALB/c mice were exposed to TS for 12 weeks, along with or without 1 mg/kg SB203580 (p38 inhibitors) treatment. Histopathological analysis, alterations in the levels of IL-33, liver CSCs markers, EMT-like changes and p38 MAPK activation in liver tissues of mice were analyzed by immunohistochemical staining, immunofluorescence assay and Western blot analysis. Moreover, LO2 immortalized human liver cells were exposed to cigarette smoke extract (CSE) and the tumorsphere formation ability was determined. LO2 cells were further treated with IL-33 or CSE and the expression of phosphorylated p38, liver CSCs markers and EMT-related proteins was examined.ResultsLong term TS exposure increased the levels of CSCs markers, induced epithelial-to mesenchymal transition (EMT) and inflammatory factor IL-33 expression. Moreover, we showed that p38 MAPK modulated TS-stimulated hepatic CSC-like properties, as evidenced by the findings that long term TS exposure activated p38, and that TS-induced stemness was abolished by p38 inhibition. In addition, data from in vitro model showed that similar to cigarette smoke extract (CSE), IL-33 treatment promoted the activation of p38, increased the levels of liver CSCs markers expression and EMT-like changes.ConclusionsCollectively, these data suggested that IL-33/p38 axis plays an important role in long term TS exposure-induced acquisition of hepatic CSC-like properties.

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“…Transient transfection was performed as previously described. 21 For overexpression of Nanog, cells were transfected with a control vector…”

Section: Transient Transfectionmentioning

confidence: 99%

Nanog mediates tobacco smoke‐induced enhancement of renal cancer stem cell properties

Zhang

Sun

et al. 2020

Environmental Toxicology

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Nanog plays an important role in the regulation of cancer stem cells (CSCs) which participate in tumorgenesis and progression. In renal cancer, tobacco smoke (TS) is considered a major risk factor. However, the molecular mechanism by which TS induces the development of renal CSC properties remains largely unknown. In this study, we showed that the level of Nanog was elevated in renal cell carcinoma (RCC) patients with a smoking history, and that Nanog overexpression promoted the traits of CSCs in renal cancer. We further demonstrated that a 8-week exposure of TS enhanced the formation of renal tumorspheres, increased the population of CD133-positive cells, and stimulated the expression of Nanog and CSC markers. In addition, TS was found to play a role in accelerating the cell growth transition from G1 to S phase in renal CSCs. Finally, we demonstrated that the TS-induced effects in renal CSCs could be reversed through the downregulation of Nanog. Our results suggested that Nanog plays a role in mediating TS-induced renal CSC properties. This study may provide new insights into the molecular mechanism of TS-related renal tumorigenesis, which can contribute to the future development of therapeutics for renal cancer.

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

Cited by 25 publications

References 44 publications

Perspectives on Wnt Signal Pathway in the Pathogenesis and Therapeutics of Chronic Obstructive Pulmonary Disease

Perspectives on Wnt Signal Pathway in the Pathogenesis and Therapeutics of Chronic Obstructive Pulmonary Disease

Tobacco smoke induced hepatic cancer stem cell-like properties through IL-33/p38 pathway

Nanog mediates tobacco smoke‐induced enhancement of renal cancer stem cell properties

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