Chemoprevention of Cigarette Smoke–Induced Alterations of MicroRNA Expression in Rat Lungs

Izzotti, Alberto; Calin, George A.; Steele, Vernon E.; Cartiglia, Cristina; Longobardi, M.; Croce, Carlo M.; Flora, Silvio De

doi:10.1158/1940-6207.capr-09-0202

Cited by 106 publications

(105 citation statements)

References 46 publications

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“…Administration of the dietary agents, Phenethyl isothiocyanate (PEITC) and Indole-3-carbinol (I3C), two major components of cruciferous vegetables, attenuated the cigarette smokeinduced down-regulation of miRNA expression. In the case of the combined treatment with PEITC and I3C, they had profound effects on almost all CS-down-regulated miRNAs and their expression even exceeded the baseline situation (59). In previous studies, PEITC was also the most effective agent in inhibition of CS-related cytogenetic damage, transcriptome alterations, and lung tumorigenesis (55,60,61).…”

Section: Anti-estrogenic Compounds As Attenuators Of Cigarette Smoke mentioning

confidence: 86%

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: Anti-estrogenic Compounds As Attenuators Of Cigarette Smoke mentioning

confidence: 86%

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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“…Among them, the upregulated miRs included let-7a, let-7b and let-7c (23). Izzotti et al (27,28) found that exposure to cigarette smoke alters miR expression in the lungs of rats. Our study demonstrated that expression of the tumor suppressors let-7a/7g was upregulated after tea catechin treatment.…”

Section: Discussionmentioning

confidence: 99%

“…In recent years, it has been reported that tea catechins induce the modification of the expression profile of miRs and mediate the apoptotic effect in human cancer cells (22,23). Furthermore, let-7 is known as a tumor suppressor in lung cancer cells or animal models by repressing cell proliferation (10,(24)(25)(26) and its expression profile may be altered by various agents (23,27,28). However, the effect and mechanism of tea catechins on let-7 expression in human lung cancer remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7

Zhong

Dong

Yang

et al. 2012

Experimental and Therapeutic Medicine

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Abstract. Green tea catechins are known to function as anticancer agents via inhibition of carcinogenesis during the initiation, promotion and progression stages. Many potential mechanisms have been proposed, yet the precise mechanism of lung cancer prevention by green tea catechins remains unclear. microRNAs (miRs) are a class of 21-24 nucleotide small non-coding RNAs and play critical roles throughout cellular development and regulation. Emerging evidence demonstrates that tea catechins influence the expression of miRs in human cancer cells to inhibit tumorigenesis. Both let-7a-1 and let-7g were detected in the human lung cancer cells treated with tea catechins. The cell viability and cell cycle were analyzed after tea catechins treatment. In the present study, we found that tea catechins upregulated the tumor-suppressor miRs, let-7a-1 and let-7g, in lung cancer cell lines. The upregulation of let-7a/7g repressed the expression of their targets, C-MYC and the regulatory protein of LIN-28, at the mRNA and protein levels. Moreover, the cell growth assay indicated that tea catechins significantly inhibited cell proliferation, and the flow cytometric analysis revealed an increase in the number of cells in the G2/M phase and a decrease in the number of cells in the S phase after treatment with tea catechins. These observations suggest that green tea catechins mediate the inhibition of proliferation of lung cancer cells through the let-7 signaling pathway.

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“…miR125b, miR-26a, miR-146-pre, let-7a, let-7c, miR-192, miR-222-pre, miR-99, and miR-123 are some of the miRNA downregulated by cigarette smoke; their expression was altered in rats treated with orally administered PEITC for 3 days prior to exposing them to cigarette smoke for 28 consecutive days (84). The effect of PEITC or glucocorticoid budesonide treatment, either alone or in combination, on miRNA expression was analyzed in the mouse liver and lungs.…”

Section: Phenethyl Isothiocyanatementioning

confidence: 99%

Plant Phytochemicals as Epigenetic Modulators: Role in Cancer Chemoprevention

Thakur

Deb

Babcook

et al. 2013

AAPS J

136

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Abstract. In recent years, "nutri-epigenetics," which focuses on the influence of dietary agents on epigenetic mechanism(s), has emerged as an exciting novel area in epigenetics research. Targeting of aberrant epigenetic modifications has gained considerable attention in cancer chemoprevention research because, unlike genetic changes, epigenetic alterations are reversible and occur during early carcinogenesis. Aberrant epigenetic mechanisms, such as promoter DNA methylation, histone modifications, and miRNA-mediated post-transcriptional alterations, can silence critical tumor suppressor genes, such as transcription factors, cell cycle regulators, nuclear receptors, signal transducers, and apoptosis-inducing and DNA repair gene products, and ultimately contribute to carcinogenesis. In an effort to identify and develop anticancer agents which cause minimal harm to normal cells while effectively killing cancer cells, a number of naturally occurring phytochemicals in food and medicinal plants have been investigated. This review highlights the potential role of plant-derived phytochemicals in targeting epigenetic alterations that occur during carcinogenesis, by modulating the activity or expression of DNA methyltransferases, histone modifying enzymes, and miRNAs. We present in detail the epigenetic mode of action of various phytochemicals and discuss their potential as safe and clinically useful chemopreventive strategies.

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Chemoprevention of Cigarette Smoke–Induced Alterations of MicroRNA Expression in Rat Lungs

Cited by 106 publications

References 46 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

Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7

Plant Phytochemicals as Epigenetic Modulators: Role in Cancer Chemoprevention

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