Alternative mechanisms of miR-34a regulation in cancer

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F17%3A00486108" target="_blank" >RIV/68081707:_____/17:00486108 - isvavai.cz</a>

Alternative codes found

RIV/00159816:_____/17:00068380 RIV/00216224:14310/17:00100427

Result on the web

<a href="http://dx.doi.org/10.1038/cddis.2017.495" target="_blank" >http://dx.doi.org/10.1038/cddis.2017.495</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/cddis.2017.495" target="_blank" >10.1038/cddis.2017.495</a>

Result language

angličtina

Original language name

Alternative mechanisms of miR-34a regulation in cancer

Original language description

MicroRNA miR-34a is recognized as a master regulator of tumor suppression. The strategy of miR-34a replacement has been investigated in clinical trials as the first attempt of miRNA application in cancer treatment. However, emerging outcomes promote the re-evaluation of existing knowledge and urge the need for better understanding the complex biological role of miR-34a. The targets of miR-34a encompass numerous regulators of cancer cell proliferation, survival and resistance to therapy. MiR-34a expression is transcriptionally controlled by p53, a crucial tumor suppressor pathway, often disrupted in cancer. Moreover, miR-34a abundance is fine-tuned by context-dependent feedback loops. The function and effects of exogenously delivered or re-expressed miR-34a on the background of defective p53 therefore remain prominent issues in miR-34a based therapy. In this work, we review p53-independent mechanisms regulating the expression of miR-34a. Aside from molecules directly interacting with MIR34A promoter, processes affecting epigenetic regulation and miRNA maturation are discussed. Multiple mechanisms operate in the context of cancer-associated phenomena, such as aberrant oncogene signaling, EMTor inflammation. Since p53-dependent tumor-suppressive mechanisms are disturbed in a substantial proportion of malignancies, we summarize the effects of miR-34a modulation in cell and animal models in the clinically relevant context of disrupted or insufficient p53 function.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

10601 - Cell biology

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2017

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Cell Death & Disease

ISSN

2041-4889

e-ISSN

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Volume of the periodical

8

Issue of the periodical within the volume

2017

Country of publishing house

GB - UNITED KINGDOM

Number of pages

10

Pages from-to

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UT code for WoS article

000414022900059

EID of the result in the Scopus database

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