SLABÁKOVÁ, Eva, Z. CULIG, Ján REMŠÍK and Karel SOUČEK. Alternative mechanisms of miR-34a regulation in cancer. CELL DEATH & DISEASE. LONDON: NATURE PUBLISHING GROUP, 2017, vol. 8, October, p. 1-10. ISSN 2041-4889. Available from: https://dx.doi.org/10.1038/cddis.2017.495.
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Basic information
Original name Alternative mechanisms of miR-34a regulation in cancer
Authors SLABÁKOVÁ, Eva (203 Czech Republic), Z. CULIG (40 Austria), Ján REMŠÍK (703 Slovakia, belonging to the institution) and Karel SOUČEK (203 Czech Republic, guarantor, belonging to the institution).
Edition CELL DEATH & DISEASE, LONDON, NATURE PUBLISHING GROUP, 2017, 2041-4889.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 10601 Cell biology
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 5.638
RIV identification code RIV/00216224:14310/17:00100427
Organization unit Faculty of Science
Doi http://dx.doi.org/10.1038/cddis.2017.495
UT WoS 000414022900059
Keywords in English EPITHELIAL-MESENCHYMAL TRANSITION; CHRONIC LYMPHOCYTIC-LEUKEMIA; TUMOR-SUPPRESSOR; PROSTATE-CANCER; MICROPROCESSOR COMPLEX; HEPATOCELLULAR-CARCINOMA; NEUROBLASTOMA-CELLS; MICRORNA EXPRESSION; MOTILE CILIOGENESIS; MIRNA BIOGENESIS
Tags NZ, rivok
Tags International impact, Reviewed
Changed by Changed by: Ing. Nicole Zrilić, učo 240776. Changed: 28/3/2018 13:26.
Abstract
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.
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