Modulation of microRNA expression by budesonide, phenethyl isothiocyanate and cigarette smoke in mouse liver and lung

Izzotti, Alberto; Larghero, Patrizia; Cartiglia, Cristina; Longobardi, M.; Pfeffer, Ulrich; Steele, Vernon E.; Flora, Silvio De

doi:10.1093/carcin/bgq037

Cited by 102 publications

(80 citation statements)

References 29 publications

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“…These findings, which support the interpretation that MCS is a strong promoting agent, are in line with our previous studies in mice exposed to MCS early in life, both in terms of molecular biomarkers (10)(11)(12)(13)(14)(15) and of tumors and other histopathological alterations (16)(17)(18)(19)(20)(21)(22). Clearly, all these studies have the limitation that the molecular analyses are done on whole tissues.…”

Section: Discussionsupporting

confidence: 90%

“…We developed suitable models for evaluating the efficacy and tolerability of chemopreventive agents in mice exposed to MCS in terms either of molecular biomarkers (10)(11)(12)(13)(14)(15) and/or of lung tumors, both benign and malignant, and other histopathological alterations in multiple organs (16)(17)(18)(19)(20)(21)(22).…”

Section: Lapatinib or N-[3-chloro-4-[(3-fluorophenyl)methoxy]phenyl]mentioning

confidence: 99%

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Assay of lapatinib in murine models of cigarette smoke carcinogenesis

et al. 2014

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Lapatinib, a dual tyrosine kinase inhibitor targeting the epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER-2), is prescribed for the treatment of patients with metastatic breast cancer overexpressing HER-2. Involvement of this drug in pulmonary carcinogenesis has been poorly investigated. We used murine models suitable to evaluate cigarette smoke-related molecular and histopathological alterations. A total of 481 Swiss H mice were used. The mice were exposed to mainstream cigarette smoke (MCS) during the first four months of life. After 10 weeks, MCS caused an elevation of bulky DNA adducts, oxidative DNA damage and an extensive downregulation of microRNAs in lung. After four months, an increase in micronucleus frequency was observed in peripheral blood erythrocytes. After 7.5 months, histopathological alterations were detected in the lung, also including benign tumors and malignant tumors, and in the urinary tract. A subchronic toxicity study assessed the non-toxic doses of lapatinib, administered daily with the diet after weaning. After 10 weeks, lapatinib significantly attenuated the MCS-related nucleotide changes and upregulated several low-intensity microRNAs in lung. The drug poorly affected the MCS systemic genotoxicity and had modest protective effects on MCS-induced preneoplastic lesions in lung and kidney, when administered under conditions that temporarily mimicked interventions either in current smokers or exsmokers. On the other hand, it caused some toxicity to the liver. Thus, on the whole, lapatinib appears to have a low impact in the smoke-related lung carcinogenesis models used, especially in terms of tumorigenic response.

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Section: Discussionsupporting

confidence: 90%

Section: Lapatinib or N-[3-chloro-4-[(3-fluorophenyl)methoxy]phenyl]mentioning

confidence: 99%

Assay of lapatinib in murine models of cigarette smoke carcinogenesis

et al. 2014

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“…These miRNAs expressed differentially were the one associated with genes regulating stress response, protein repair, cell proliferation, and inflammation. No study on the effect of PEITC on miRNA expression in cancer has been reported so far (85).…”

Section: Phenethyl Isothiocyanatementioning

confidence: 99%

Plant Phytochemicals as Epigenetic Modulators: Role in Cancer Chemoprevention

Thakur

Deb

Babcook

et al. 2013

AAPS J

141

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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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“…Environmental factors (EFs) have recently been utilized as new means of inferring the relationship between diseases and miRNAs. The miREnvironment database contains information of EFs, such as drugs [6], cigarettes [7], alcohol [8], viruses [9], stress [10], and radiation [11], which plays a significant role in affecting various diseases. By applying the propagation algorithm on the miRNA-miRNA similarity network, we found hidden potential to identify association between disease-miRNA.…”

Section: Introductionmentioning

confidence: 99%

A method of extracting disease-related microRNAs through the propagation algorithm using the environmental factor based global miRNA network

Kim

Yong-Jin

et al. 2015

BME

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Abstract. MicroRNAs (miRNA) are known to be involved in the development of various diseases. Hence various scientists in the field have been utilized computational analyses to determine the relationship between miRNA and diseases. However, the knowledge of miRNA and disease is still very limited. Therefore, we combined Environmental Factor (EF) data to a miRNA global network. Increasing research has shown that relationship between miRNAs and EFs play a significant role in classifying types of diseases. Environmental Factors consist of radiation, drugs, viruses, alcohol, cigarettes, and stress. Our global network considered all the interactions between every pair of miRNAs, which has led to precise analyses in comparison to local networks. As a result, our approaches' performance demonstrated its effectiveness in identifying diseaserelated miRNA and this is the area under the ROC curve (AUC) of 74.46%. Furthermore, comparative experiment has shown that our approach performs comparable to other existing methods with an accuracy of 94%, 90% and 96% for breast cancer, colonic cancer, and lung cancer respectively. In conclusion, these results support that our research has broadened new biological insights on identifying disease-related miRNAs.

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Modulation of microRNA expression by budesonide, phenethyl isothiocyanate and cigarette smoke in mouse liver and lung

Cited by 102 publications

References 29 publications

Assay of lapatinib in murine models of cigarette smoke carcinogenesis

Assay of lapatinib in murine models of cigarette smoke carcinogenesis

Plant Phytochemicals as Epigenetic Modulators: Role in Cancer Chemoprevention

A method of extracting disease-related microRNAs through the propagation algorithm using the environmental factor based global miRNA network

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