Interplay between histopathological alterations, cigarette smoke and chemopreventive agents in defining microRNA profiles in mouse lung

Izzotti, Alberto; Larghero, Patrizia; Balansky, Roumen; Pfeffer, Ulrich; Steele, Vernon E.; Flora, Silvio De

doi:10.1016/j.mrfmmm.2010.10.003

Cited by 37 publications

(54 citation statements)

References 58 publications

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“…The observation of a global miRNA repression in the lungs of rodents exposed to CS has also been reported (49)(50)(51)(52). Izzotti et al show in their results the extensive down-regulation of 126 miRNAs in lungs of rats, 4 weeks after CS exposure (49).…”

Section: Mirnas Repression By Cigarette Smoke In the Lungsmentioning

confidence: 65%

A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer

Cohen

Burgos-Aceves²,

Smith³

2016

Transl. Lung Cancer Res.

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Alteration in the expression of microRNAs (miRNAs) is associated with oncogenesis and cancer progression. In this review we aim to suggest that elevated levels of estrogens and their metabolites inside the lungs as a result of cigarette smoke exposure can cause widespread repression of miRNA and contribute to lung tumor development. Anti-estrogenic compounds, such as the components of cruciferous vegetables, can attenuate this effect and potentially reduce the risk of lung cancer (LC) among smokers. (Table 1), and seem to work differently depending on the cellular context (47). However, developing any type of LC by deregulation of miRNAs via ER-Estrogen effect is still not entirely clear (8). miRNAs repression by cigarette smoke in the lungsWe have summarized before the results showing reduced expression levels of miRNAs in various tumors and cancer cell lines, including LC (48). The observation of a global miRNA repression in the lungs of rodents exposed to CS has also been reported (49)(50)(51)(52). Izzotti et al. show in their results the extensive down-regulation of 126 miRNAs in lungs of rats, 4 weeks after CS exposure (49). Such a short-lasting exposure to CS resulted in reversible miRNA alterations, as miRNA down-regulation was considerably attenuated one week after smoking cessation (51). By contrast, the repression of miRNA detected in mice exposed to CS for 4 months still persisted 3 months after smoking cessation, with the progressive development of cancer in the lung, suggesting that long-lasting exposure is needed to induce irreversible miRNA alterations (51,53). In their previous published results, using the same animal model, Izzotti et al. have found that CS up-regulates gene transcription and protein expression (54,55). The authors suggested that the CS-induced down-regulation of miRNA cause oncogene activation and cell proliferation, and that the persistence of these molecular alterations is crucial to commit lung cells towards carcinogenesis (51,53). These results are supported by the study of Schembri et al., who found that most of the differentially expressed miRNAs in the human bronchial airway epithelium were downregulated in smokers and were inversely correlated with their predicted targets (56). The same phenomenon was also observed in alveolar macrophages of smokers, where CS decreased global miRNA expression, while increased their predicted targets (57). In this later study the decrease in global miRNA expression was more pronounced in heavy smokers, suggesting that the magnitude of miRNA repression is related to the extent of smoking history (57). Anti-estrogenic compounds as attenuators of cigarette smoke effectsStudies suggest that phytochemicals from vegetables and fruits exhibit chemopreventive activities against various types of cancer (58). Izzotti et al. (59) evaluated miRNA expression in the lungs of rats exposed to CS and treated with several cancer chemopreventive agents. Administration of the dietary agents, Phenethyl isothiocyanate (PEITC) and Indole-3-carbi...

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Section: Mirnas Repression By Cigarette Smoke In the Lungsmentioning

confidence: 65%

A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer

Cohen

Burgos-Aceves²,

Smith³

2016

Transl. Lung Cancer Res.

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“…After reaching confl uence, media were changed, human airway epithelium and reported that miR-218 and miR-128b were decreased in expression. Xi et al 6 showed that cigarette smoke condensate increased the expression of miR-31 in airway cells, and Izzotti et al 7 investigated the impact of cigarette smoking on mouse lungs. miRNAs are likely to play a role in the pathogenesis of lung cancer, 8 and involvement of miRNA let-7d has been suggested in idiopathic pulmonary fibrosis.…”

Section: Cell Culturementioning

confidence: 99%

MicroRNA-199a-5p Is Associated With Hypoxia-Inducible Factor-1α Expression in Lungs From Patients With COPD

Mizuno

Bogaard

Gomez-Arroyo

et al. 2012

Chest

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MicroRNAs (miRNAs) are noncoding RNA molecules that modulate gene expression by binding to complementary sequences in the coding-or the 3 9 -untranslated region of target mRNAs. miRNAs Background: MicroRNAs (miRNAs) are small noncoding RNAs that silence target gene expression posttranscriptionally, and their impact on gene expression has been reported in various diseases. It has been reported that the expression of the hypoxia-inducible factor-1 a (HIF-1 a ) is reduced and that of p53 is increased in lungs from patients with COPD. However, the role of miRNAs associated with these genes in lungs from patients with COPD is unknown. Methods: Lung tissue samples from 55 patients were included in this study. Total RNA, miRNA, and protein were extracted from lung tissues and used for reverse transcriptase polymerase chain reaction and Western blot analysis. Cell culture experiments were performed using cultured human pulmonary microvascular endothelial cells (HPMVECs). Results: miR-34a and miR-199a-5p expressions were increased, and the phosphorylation of AKT was decreased in the lung tissue samples of patients with COPD. The miR-199a-5p expression was correlated with HIF-1 a protein expression in the lungs of patients with COPD. Transfection of HPMVECs with the miR-199a-5p precursor gene decreased HIF-1 a protein expression, and transfection with the miR-34a precursor gene increased miR-199a-5p expression. Conclusions: These data suggest that miR-34a and miR-199a-5p contribute to the pathogenesis of COPD, and these miRNAs may also affect the HIF-1 a -dependent lung structure maintenance program.CHEST 2012; 142(3):663-672Abbreviations: GOLD 5 Global Initiative for Chronic Obstructive Lung Disease; HIF-1 a 5 hypoxia-inducible factor-1 a ; HPMVEC 5 human pulmonary microvascular endothelial cell; LTRC 5 Lung Tissue Repository Consortium; miRNA 5 microRNA; pAKT 5 phosphorylated AKT; PVDF 5 polyvinylidene difl uoride; RT-PCR 5 reverse transcriptase polymerase chain reaction; siRNA 5 small interfering RNA; VEGF 5 vascular endothelial growth factor

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“…Several studies have recently demonstrated that exposure to cigarette smoking in human and animal models causes alternations in miRNAs expression (Izzotti et al, 2009(Izzotti et al, , 2011Schembri et al, 2009;Seike et al, 2009). Dysregulation of the miRNAs is closely related with an altered expression of their target mRNA, and therefore may be implicated with carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Altered Expression of miRNAs Is Related to Larynx Cancer TNM Stage and Patients' Smoking Status

Bruzgielewicz

Osuch-WojcikiewiczEwa

NiemczykKazimierz

et al. 2017

DNA and Cell Biology

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It has been reported that microRNAs (miRNAs) are responsible for acquiring all the hallmarks of cancer cells, as well as have a significant impact on the clinical management of cancers at every stage, including prognosis, remission, relapse, and metastasis. In this study, we investigated the association of miR-29a-3p, miR-202-3p, miR-3713, miR-4768-3p, and miR-548aa expression with clinicopathologic features in patients suffering from laryngeal cancer (LC) and determined the potential role of studied miRNAs in the progression of LC. The study group consisted of 48 patients with untreated primary tumors of head and neck cancer localized in the larynx. Expression of the selected miRNAs was verified by the qRT-PCR technique. We showed that the expression of miR-29a as well as miR-548aa was positively correlated with tumor stage and lymph node metastasis, whereas the expression of miR-4768-3p was negatively correlated with lymph node metastasis. Furthermore, we investigated that exposure to cigarette smoke altered miRNA expression profile in LC. The expression level of miR-202-3p was significantly increased in smoking patients compared with nonsmokers, whereas the miR-4768-3p, miR-548aa, and miR-3713 were markedly decreased. Our research contributed toward better elucidating the mechanisms underlying the progression of LC as well as the use of miRNAs inhibitors as novel agents against progression and metastasis of LC.

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Interplay between histopathological alterations, cigarette smoke and chemopreventive agents in defining microRNA profiles in mouse lung

Cited by 37 publications

References 58 publications

A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer

A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer

MicroRNA-199a-5p Is Associated With Hypoxia-Inducible Factor-1α Expression in Lungs From Patients With COPD

Altered Expression of miRNAs Is Related to Larynx Cancer TNM Stage and Patients' Smoking Status

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