&lt;p&gt;Tobacco Smoke Plays an Important Role in Initiation and Development of Lung Cancer by Promoting the Characteristics of Cancer Stem Cells&lt;/p&gt;

Lü, Ling; Liang, Qiaoyan; Shen, Shiyue; Feng, Lei; Jin, Longtao; Zhao, Liang

doi:10.2147/cmar.s272277

Cited by 9 publications

(9 citation statements)

References 34 publications

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“…TS is the leading cause of lung cancer and promotes initiation and progression of pulmonary tumorigenesis ( 5 – 7 , 9 , 48 ). The underlying molecular mechanism of TS causing lung cancer remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Liang

Zhang

et al. 2022

Oncol Lett

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Tobacco smoke (TS) is the major cause of lung cancer. The abnormal proliferation and epithelial-mesenchymal transition (EMT) of lung cells promote occurrence and development of lung cancer. The p38 pathway intervenes in this cancer development. Hesperidin also serves a role in human health and disease prevention. The roles of p38 in TS-mediated abnormal cell proliferation and EMT, and the hesperidin intervention thereof are not yet understood. In the present study, it was demonstrated that TS upregulated proliferating cell nuclear antigen, vimentin and N-cadherin expression, whereas it downregulated E-cadherin expression, as assessed using western blotting and reverse transcription-quantitative PCR. Furthermore, it was observed that inhibition of the p38 pathway inhibit TS-induced proliferation and EMT. Hesperidin treatment prevented the TS-induced activation of the p38 pathway, EMT and cell proliferation in mouse lungs. The findings of the present study may provide insights into the pathogenesis of TS-related lung cancer.

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Section: Discussionmentioning

confidence: 99%

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Liang

Zhang

et al. 2022

Oncol Lett

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“…Garnering much research attention, natural compounds were recently reported to produce a suppressive effect on CSC phenotype and related regulatory pathways [ 24 , 32 , 51 ]. Due to the crucial role of CSCs in initiation and maintenance of lung cancer [ 52 ], the results herein revealing anticancer activity of TDB, a bibenzyl extracted from D. ellipsophyllum , against lung CSCs could guide the future investigations and innovations related to CSC-targeted therapy.…”

Section: Discussionmentioning

confidence: 99%

“…In vivo evidence suggests that Akt-driven CSC enrichment is mediated by activation of the Wnt/ β -catenin pathway through GSK3 β phosphorylation [ 56 ]. It has been reported that tobacco smoke, an important risk factor for lung cancer, stimulates the Wnt/ β -catenin pathway and enhances the CSC phenotype in lung cancer patients [ 52 ]. Interestingly, small molecules derived from natural products are deemed to possess much therapeutic potential and were even observed to inhibit CSC subpopulations and abolish tumor growth in vivo through inhibition of the Wnt/ β -catenin pathway [ 57 , 58 ].…”

Section: Discussionmentioning

confidence: 99%

Stemness-Suppressive Effect of Bibenzyl from Dendrobium ellipsophyllum in Human Lung Cancer Stem-Like Cells

Taweecheep

Khine

Hlosrichok

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Cancer stem-like cells (CSCs) are key mediators driving tumor initiation, metastasis, therapeutic failure, and subsequent cancer relapse. Thus, targeting CSCs has recently emerged as a potential strategy to improve chemotherapy. In this study, the anticancer activity and stemness-regulating capacity of 4,5,4′-trihydroxy-3,3′-dimethoxybibenzyl (TDB), a bibenzyl extracted from Dendrobium ellipsophyllum, are revealed in CSCs of various human lung cancer cells. Culture with TDB (5–10 μM) strongly abolished tumor-initiating cells in lung cancer H460, H23, and A549 cells in both anchorage-dependent and anchorage-independent colony formation assays. Through the 3D single-spheroid formation model, attenuation of self-renewal capacity was observed in CSC-enriched populations treated with 1–10 μM TDB for 7 days. Flow cytometry analysis confirmed the attenuation of %cell overexpressing CD133, a CSC biomarker, in TDB-treated lung cancer spheroids. TDB at 5–10 μM remarkably suppressed regulatory signals of p-Akt/Akt, p-GSK3β/GSK3β, and β-catenin corresponding to the downregulated mRNA level of stemness transcription factors including Nanog, Oct4, and Sox2. Moreover, the antiapoptosis Bcl-2 and Mcl-1 proteins, which are downstream molecules of Akt signaling, were evidently decreased in CSC-enriched spheroids after culture with TDB (1–10 μM) for 24 h. Interestingly, the diminution of Akt expression by specific siAkt effectively reversed suppressive activity of TDB targeting on the CSC phenotype in human lung cancer cells. These findings provide promising evidence of the inhibitory effect of TDB against lung CSCs via suppression of Akt/GSK3β/β-catenin cascade and related proteins, which would facilitate the development of this bibenzyl natural compound as a novel CSC-targeted therapeutic approach for lung cancer treatment.

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“…Also in a murine model, long-term cigarette smoke exposure in vivo lowered MSCs and HSCs, while increased gene expression related to proliferation, in what is another warning for the use of stem cells from smokers (Siggins et al 2014). Smoke is capable of induce stem cells in the route to lung cancer development (Lu et al 2020). Chronic nicotine exposition modulates epigenome through ROS induction and favors stemness in Hk-2 human kidney epithelial cells, during nicotine-related kidney carcinogenesis (Chang and Singh 2019).…”

Section: Toxic Habits and Diseases In The Donorsmentioning

confidence: 99%

A Multilevel Approach to the Causes of Genetic Instability in Stem Cells

González

2022

Handbook of Stem Cell Therapy

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This chapter addresses the genetic instability in stem cells, a central feature that is an important determinant for the safety and effectiveness of cell-based therapies. First, DNA damage response mechanism and the gene network that regulates the DNA integrity homeostasis are revisited, focusing on relationship between genetic integrity and stemness maintenance. Also, several factors have been included that influence genetic instability in vivo, i.e., ROS generation and inflammation, and in vitro regarding cell isolation, culture conditions, i.e., oxygen levels and the use of feeder layers and different carriers, splitting procedures, passage number, etc. Telomere shortening, replicative senescence aneuploidy, and the senescence-associated secretory phenotype are different processes involved in deterioration of stem cells abilities for homing, reparability, and paracrine modulation. Moreover, less effective DNA repair upon senescence increases the propensity of developing tumors for stem cells that is one the main concerns related to genetic instability in stem cells. Nuclear organization and their determinants linked to chromosome aberrations and aneuploidy in stem cells and those epigenetic changes affecting stability are addressed. Differences between adipose, embryonic, and induced pluripotent stem cells are analyzed regarding to their ontogeny, changes in culture, and variation in proliferative capacity and stemness. The effect of reprogramming methods in genetic instability and variation in mutagenicity according to genes utilized for pluripotency induction, i.e., Yamanaka's factors and others, is discussed. Donor-related factors, i.e., age, smoking, and alcohol consumption, comorbidities, i.e., obesity, insulin resistance, diabetes, are mentioned for wide evaluation of genetic instability. The next years must witness consensus protocols that will contribute to control the effects of factors that alter stem cell genetic stability to increase the security and applicability of cell-based therapy.

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<p>Tobacco Smoke Plays an Important Role in Initiation and Development of Lung Cancer by Promoting the Characteristics of Cancer Stem Cells</p>

Cited by 9 publications

References 34 publications

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Hesperidin inhibits tobacco smoke‑induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway

Stemness-Suppressive Effect of Bibenzyl from Dendrobium ellipsophyllum in Human Lung Cancer Stem-Like Cells

A Multilevel Approach to the Causes of Genetic Instability in Stem Cells

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