MicroRNAs-Role in Lung Cancer

Guz, Małgorzata; Rivero-Müller, Adolfo; Okon, Estera; Stenzel-Bembenek, Agnieszka; Polberg, Krzysztof; Słomka, Maria; Stepulak, Andrzej

doi:10.1155/2014/218169

Cited by 64 publications

(49 citation statements)

References 176 publications

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“…Increasing evidence has suggested that miRNAs are involved in a number of biological processes, including development, differentiation, apoptosis, metabolism, immunity and tumor progression (5,(7)(8)(9). In addition, a growing body of evidence strongly suggests that the dysregulation or dysfunction of miRNAs may modulate tumor initiation and progression, and may participate in tumor cell invasion and metastasis (5,(9)(10)(11)(12)(13)(14). miRNAs may function as oncogenes or tumor suppressors depending on their specific target genes (15).…”

Section: Introductionmentioning

confidence: 99%

miR-154 inhibits migration and invasion of human non-small cell lung cancer by targeting ZEB2

et al. 2016

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Abstract. Emerging evidence suggests that microRNAs (miRs) play critical roles in the development and progression of non-small cell lung cancer (NSCLC). In a previous study, the present authors demonstrated that miR-154 acts as a tumor suppressor in NSCLC; however, its underlying molecular mechanism and target in NSCLC remain poorly understood. In the present study, ectopic expression of miR-154 remarkably suppressed cell migration and invasion in NSCLC cells.Zinc finger E-box binding homeobox 2 (ZEB2) was identified as a direct target of miR-154 in NSCLC cells. Furthermore, overexpression of miR-154 could decrease the expression of ZEB2 at the messenger RNA and protein levels. Ectopic expression of miR-154 also increased the levels of E-cadherin, an epithelial marker, and decreased the levels of vimentin, a mesenchymal marker, which contributed to suppress epithelial-mesenchymal transition (EMT) and to inhibit cell migration and invasion. In addition, downregulation of ZEB2 exerted similar effects to those caused by miR-154 overexpression on NSCLC cell migration and invasion, while upregulation of ZEB2 could significantly reverse the inhibitory effects on migration and invasion caused by miR-154 on NSCLC cells. These findings demonstrated that miR-154 inhibited migration and invasion of NSCLC cells by regulating EMT through targeting ZEB2, suggesting that miR-154 may be a potential anticancer therapeutic target for NSCLC.

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Section: Introductionmentioning

confidence: 99%

miR-154 inhibits migration and invasion of human non-small cell lung cancer by targeting ZEB2

et al. 2016

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“…A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer regulated (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).…”

Section: Mini-reviewmentioning

confidence: 99%

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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“…Over the past decade, a class of small, non-coding, singlestranded RNAs known as microRNAs (miRNAs) have emerged as major regulators of the initiation and progression of human cancers, including lung cancer (24,25). The up-regulation of oncogenic miRNAs (targeting tumor suppressor genes) and the down-regulation of tumor-suppressive miRNAs (targeting oncogenes) lead to the dysfunction of cancer cells, including malignant proliferation, invasion, and metastasis (26 -28).…”

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confidence: 99%

miR-193a-3p Functions as a Tumor Suppressor in Lung Cancer by Down-regulating ERBB4

Liang

Liu

Yan

et al. 2015

Journal of Biological Chemistry

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Background: ERBB4 plays an important role in the etiology and progression of lung cancer. Results: miR-193a-3p suppressed proliferation and invasion and promoted apoptosis in lung cancer cells and xenograft mice by negatively regulating ERBB4. Conclusion: miR-193a-3p exerted an anti-tumor effect by negatively regulating ERBB4 in lung cancer. Significance:This study may open new avenues for future lung cancer therapies.

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MicroRNAs-Role in Lung Cancer

Cited by 64 publications

References 176 publications

miR-154 inhibits migration and invasion of human non-small cell lung cancer by targeting ZEB2

miR-154 inhibits migration and invasion of human non-small cell lung cancer by targeting ZEB2

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

miR-193a-3p Functions as a Tumor Suppressor in Lung Cancer by Down-regulating ERBB4

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