The interplay between transcription factors and microRNAs in genome‐scale regulatory networks

Martínez, Natàlia; Walhout, Albertha J.M.

doi:10.1002/bies.200800212

Cited by 240 publications

(207 citation statements)

References 105 publications

(118 reference statements)

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“…Tumor cells, where miR-146b is highly up-regulated, may well be making use of such efficient mechanisms to aberrantly exploit them favoring dedifferentiation and progression. At the genome scale level, it is well established that these regulatory circuits involving miRNAs and transcription factors are prevalent mechanisms of gene expression (44,46). The regulatory circuit miR-146b-3p-PAX8-NIS described above illustrates the importance of such regulatory miRNA-TFs pairs as examples of regulators of essential biological functions like the metabolism of iodide and ultimately dedifferentiated state in thyroid cells (Fig.…”

Section: From Cancer Genes To Signaling and Differentiation: Toward Amentioning

confidence: 97%

“…In addition, PAX8 regulates miR-146b transcription forming a regulatory negative feedback loop where PAX8 limits its own activity by inducing a repressor, miR-146b. Such a loop can result in coexpression of both components, either in steady-state levels or in oscillation (44). Therefore, the balanced expression of both components depends on additional input signals.…”

Section: From Cancer Genes To Signaling and Differentiation: Toward Amentioning

confidence: 99%

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ENDOCRINE TUMOURS: Advances in the molecular pathogenesis of thyroid cancer: lessons from the cancer genome

Riesco‐Eizaguirre

Santisteban

2016

European Journal of Endocrinology

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Thyroid cancer is the most common endocrine malignancy giving rise to one of the most indolent solid cancers, but also one of the most lethal. In recent years, systematic studies of the cancer genome, most importantly those derived from The Cancer Genome Altas (TCGA), have catalogued aberrations in the DNA, chromatin, and RNA of the genomes of thousands of tumors relative to matched normal cellular genomes and have analyzed their epigenetic and protein consequences. Cancer genomics is therefore providing new information on cancer development and behavior, as well as new insights into genetic alterations and molecular pathways. From this genomic perspective, we will review the main advances concerning some essential aspects of the molecular pathogenesis of thyroid cancer such as mutational mechanisms, new cancer genes implicated in tumor initiation and progression, the role of non-coding RNA, and the advent of new susceptibility genes in thyroid cancer predisposition. This look across these genomic and cellular alterations results in the reshaping of the multistep development of thyroid tumors and offers new tools and opportunities for further research and clinical development of novel treatment strategies.

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Section: From Cancer Genes To Signaling and Differentiation: Toward Amentioning

confidence: 97%

Section: From Cancer Genes To Signaling and Differentiation: Toward Amentioning

confidence: 99%

ENDOCRINE TUMOURS: Advances in the molecular pathogenesis of thyroid cancer: lessons from the cancer genome

Riesco‐Eizaguirre

Santisteban

2016

European Journal of Endocrinology

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“…Previous studies have suggested an interplay between transcription factors and miRNAs in genome-wide regulatory networks. 83 Targeting of transcription factors by miRNAs could have a global impact on TLR-induced gene expression. NF-kB is the most important transcription factor in the TLR signaling pathway.…”

Section: Mirnas In Regulation Of Tlr and Rig-i Pathways Yk LI And Xy mentioning

confidence: 99%

MicroRNAs in the regulation of TLR and RIG-I pathways

2012

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The innate immune system recognizes invading pathogens through germline-encoded pattern recognition receptors (PRRs), which elicit innate antimicrobial and inflammatory responses and initiate adaptive immunity to control or eliminate infection. Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I) are the key innate immune PRRs and are tightly regulated by elaborate mechanisms to ensure a beneficial outcome in response to foreign invaders. Although much of the focus in the literature has been on the study of protein regulators of inflammation, microRNAs (miRNAs) have emerged as important controllers of certain features of the inflammatory process. Several miRNAs are induced by TLR and RIG-I activation in myeloid cells and act as feedback regulators of TLR and RIG-I signaling. In this review, we comprehensively discuss the recent understanding of how miRNA networks respond to TLR and RIG-I signaling and their role in the initiation and termination of inflammatory responses. Increasing evidence also indicates that both virus-encoded miRNAs and cellular miRNAs have important functions in viral replication and host anti-viral immunity.

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“…Within the transcriptional and post-transcriptional trans-regulatory elements that make up gene regulatory networks, transcription factors often interact with microRNAs (miRNAs) to control gene expression [2,3]. miRNAs are post-transcriptional regulators that are expressed in a tissue-specific or developmental stage-specific manner, thereby greatly contributing to cell/tissue-specific protein expression profiles, including during lung organogenesis [4,5].…”

Section: Introductionmentioning

confidence: 99%

Transcription factors and miRNAs that regulate fetal to adultCFTRexpression change are new targets for cystic fibrosis

Viart¹,

Bergougnoux²,

Bonini³

et al. 2014

Eur Respir J

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The CFTR gene displays a tightly regulated tissue-specific and temporal expression. Mutations in this gene cause cystic fibrosis (CF). In this study we wanted to identify trans-regulatory elements responsible for CFTR differential expression in fetal and adult lung, and to determine the importance of inhibitory motifs in the CFTR-3′UTR with the aim of developing new tools for the correction of disease-causing mutations within CFTR.We show that lung development-specific transcription factors (FOXA, C/EBP) and microRNAs (miR-101, miR-145, miR-384) regulate the switch from strong fetal to very low CFTR expression after birth. By using miRNome profiling and gene reporter assays, we found that miR-101 and miR-145 are specifically upregulated in adult lung and that miR-101 directly acts on its cognate site in the CFTR-3′UTR in combination with an overlapping AU-rich element. We then designed miRNA-binding blocker oligonucleotides (MBBOs) to prevent binding of several miRNAs to the CFTR-3′UTR and tested them in primary human nasal epithelial cells from healthy individuals and CF patients carrying the p.Phe508del CFTR mutation. These MBBOs rescued CFTR channel activity by increasing CFTR mRNA and protein levels.Our data offer new understanding of the control of the CFTR gene regulation and new putative correctors for cystic fibrosis. @ERSpublications Transcription factors/miRNAs that regulate fetal to adult CFTR expression change are new targets for CF treatment

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The interplay between transcription factors and microRNAs in genome‐scale regulatory networks

Cited by 240 publications

References 105 publications

ENDOCRINE TUMOURS: Advances in the molecular pathogenesis of thyroid cancer: lessons from the cancer genome

ENDOCRINE TUMOURS: Advances in the molecular pathogenesis of thyroid cancer: lessons from the cancer genome

MicroRNAs in the regulation of TLR and RIG-I pathways

Transcription factors and miRNAs that regulate fetal to adultCFTRexpression change are new targets for cystic fibrosis

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