Cigarette smoke condensate promotes pro‐tumourigenic stromal–epithelial interactions by suppressing miR‐145

Melling, Genevieve E; Hinsley, Emma E.; Kabir, Tasnuva D.; Colley, Helen; Lambert, D

doi:10.1111/jop.12017

Cited by 22 publications

(13 citation statements)

References 21 publications

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“…Using the miRanda algorithm, we found that TUG1 binds to miR‐145‐5p. It was shown that the expression of miR‐145‐5p significantly diminished in response to a CS condensate and negatively regulated proinflammatory cytokine release from airway smooth‐muscle cells in COPD by targeting SMAD3 . In the present study, we found that CSE treatment down‐regulated miR‐145‐5p in HBE cells and lung fibroblasts, and this effect was reversed by TUG1 knockdown.…”

Section: Discussionsupporting

confidence: 60%

Long non‐coding RNA TUG1 promotes airway remodelling by suppressing the miR‐145‐5p/DUSP6 axis in cigarette smoke‐induced COPD

Yuan

Wang

et al. 2019

J Cellular Molecular Medi

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Chronic obstructive pulmonary disease (COPD) is a progressive lung disease that is primarily caused by cigarette smoke (CS)‐induced chronic inflammation. In this study, we investigated the function and mechanism of action of the long non‐coding RNA (lncRNA) taurine‐up‐regulated gene 1 (TUG1) in CS‐induced COPD. We found that the expression of TUG1 was significantly higher in the sputum cells and lung tissues of patients with COPD as compared to that in non‐smokers, and negatively correlated with the percentage of predicted forced expiratory volume in 1 second. In addition, up‐regulation of TUG1 was observed in CS‐exposed mice, and knockdown of TUG1 attenuated inflammation and airway remodelling in a mouse model. Moreover, TUG1 expression was higher in CS extract (CSE)‐treated human bronchial epithelial cells and lung fibroblasts, whereas inhibition of TUG1 reversed CSE‐induced inflammation and collagen deposition in vitro. Mechanistically, TUG1 promoted the expression of dual‐specificity phosphatase 6 (DUSP6) by sponging miR‐145‐5p. DUSP6 overexpression reversed TUG1 knockdown‐mediated inhibition of inflammation and airway remodelling. These findings suggested an important role of TUG1 in the pathological alterations associated with CS‐mediated airway remodelling in COPD. Thus, TUG1 may be a promising therapeutic target in CS‐induced airway inflammation and fibroblast activation.

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Section: Discussionsupporting

confidence: 60%

Long non‐coding RNA TUG1 promotes airway remodelling by suppressing the miR‐145‐5p/DUSP6 axis in cigarette smoke‐induced COPD

Yuan

Wang

et al. 2019

J Cellular Molecular Medi

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“…Overexpression of miR-23a has also been observed in betel nut chewers with OSCC [164,165]. Cigarette smoke condensate has been shown to have a tumourigenic effect associated with suppression of miRNA-145 in OSCC cells [166]. Nicotine has also been associated with the upregulation of miR-9 and downregulation of miR-101 in HNSCC cell lines [128].…”

Section: Carcinogen-related Mirnasmentioning

confidence: 96%

MicroRNAs and head and neck cancer: Reviewing the first decade of research

Sethi¹,

Wright²,

Wood³

et al. 2014

European Journal of Cancer

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“…Overexpression of miR-23a was described in HNSCC from areca-nut chewing patients and correlated with an increase of the DNA damage marker γH2A.X and a reduction of DBS repair [ 148 ]. A recent study reported that the downregulation of miR-145 in oral fibroblasts exposed to cigarette smoke condensates promoted pro-tumorigenic stromal-epithelial interactions [ 149 ]. A number of aberrantly expressed miRNAs were identified in HNSCC patients, who were subdivided into non-drinkers, light, and heavy drinkers.…”

Section: Ncrna Involvement In Opsccmentioning

confidence: 99%

Novel insights into epigenetic drivers of oropharyngeal squamous cell carcinoma: role of HPV and lifestyle factors

et al. 2017

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In the last years, the explosion of high throughput sequencing technologies has enabled epigenome-wide analyses, allowing a more comprehensive overview of the oropharyngeal squamous cell carcinoma (OPSCC) epigenetic landscape. In this setting, the cellular pathways contributing to the neoplastic phenotype, including cell cycle regulation, cell signaling, DNA repair, and apoptosis have been demonstrated to be potential targets of epigenetic alterations in OPSCC. Of note, it has becoming increasingly clear that HPV infection and OPSCC lifestyle risk factors differently drive the epigenetic machinery in cancer cells. Epigenetic changes, including DNA methylation, histone modifications, and non-coding RNA expression, can be used as powerful and reliable tools for early diagnosis of OPSCC patients and improve prognostication. Since epigenetic changes are dynamic and reversible, epigenetic enzymes may also represent suitable targets for the development of more effective OPSCC therapeutic strategies. Thus, this review will focus on the main known epigenetic modifications that can occur in OPSCC and their exploitation as potential biomarkers and therapeutic targets. Furthermore, we will address epigenetic alterations to OPSCC risk factors, with a particular focus on HPV infection, tobacco exposure, and heavy alcohol consumption.

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Cigarette smoke condensate promotes pro‐tumourigenic stromal–epithelial interactions by suppressing miR‐145

Abstract: These findings suggest that tobacco constituents influence the expression of miRNA within oral fibroblasts promoting a phenotype that increases oral cancer migration and sheds new light on the mechanisms underlying oral cancer pathogenesis.

Cited by 22 publications

References 21 publications

Long non‐coding RNA TUG1 promotes airway remodelling by suppressing the miR‐145‐5p/DUSP6 axis in cigarette smoke‐induced COPD

Long non‐coding RNA TUG1 promotes airway remodelling by suppressing the miR‐145‐5p/DUSP6 axis in cigarette smoke‐induced COPD

MicroRNAs and head and neck cancer: Reviewing the first decade of research

Novel insights into epigenetic drivers of oropharyngeal squamous cell carcinoma: role of HPV and lifestyle factors

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