Role of microRNA in epithelial to mesenchymal transition and metastasis and clinical perspectives
Entity
UAM. Departamento de BioquímicaPublisher
Dove Medical Press LimitedDate
2014-04-25Citation
10.2147/CMAR.S38156
Cancer Management and Research 6.1 (2014): 205-216
ISSN
1179-1322 (online); 0190-0129 (print)DOI
10.2147/CMAR.S38156Funded by
AC is funded by grants of the Spanish Ministry of Economy and Competitiveness, formerly Innovation and Sciences, (SAF2010-21143; Consolider-Ingenio CSD2007-00017) and Association for International Cancer Research (grant 12-1057). GMB is funded by SAF2010-20175, AECC-2011 and Instituto de Salud Carlos III (ISCIII) PI13/00132. GMB and AC are funded by the Community of Madrid (S2010/BMD-2303) and the Instituto de Salud Carlos III (RETIC-RD12/0036/0007). ADL is a postdoctoral researcher funded by the Sara Borrell program (ISCIII).Project
Comunidad de Madrid. S2010/BMD-2303/RECAREEditor's Version
http://dx.doi.org/10.2147/CMAR.S38156Subjects
Cancer; EMT; MET; Metastasis; microRNAs; MedicinaRights
© 2014 Díaz-López et al.Abstract
The microRNAs (miRNAs) are a class of small, 20–22 nucleotides in length, endogenously expressed noncoding RNAs that regulate multiple targets posttranscriptionally. Interestingly, miRNAs have emerged as regulators of most physiological and pathological processes, including metastatic tumor progression, in part by controlling a reversible process called epithelial-to-mesenchymal transition (EMT). The activation of EMT increases the migratory and invasive properties fundamental for tumor cell spread while activation of the reverse mesenchymal-to-epithelial transition is required for metastasis outgrowth. The EMT
triggering leads to the activation of a core of transcription factors (EMT-TFs) – SNAIL1/SNAIL2, bHLH (E47, E2-2, and TWIST1/TWIST2), and ZEB1/ZEB2 – that act as E-cadherin repressors and, ultimately, coordinate EMT. Recent evidence indicates that several miRNAs regulate the expression of EMT-TFs or EMT-activating signaling pathways. Interestingly, some miRNAs and EMT-TFs form tightly interconnected negative feedback loops that control epithelial cell plasticity, providing self-reinforcing signals and robustness to maintain the epithelial or mesenchymal cell status. Among the most significant feedback loops, we focus on the ZEB/miR-200 and the SNAIL1/miR-34 networks that hold a clear impact in the regulation of the epithelial-mesenchymal state. Recent insights into the p53 modulation of the EMT-TF/miRNA loops and epigenetic regulatory mechanisms in the context of metastasis dissemination will also
be discussed. Understanding the regulation of EMT by miRNAs opens new avenues for the diagnosis and prognosis of tumors and identifies potential therapeutic targets that might help to negatively impact on metastasis dissemination and increasing patient survival
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Google Scholar:Díaz-López, Antonio
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Moreno Bueno, Gema
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Cano, Amparo
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