Effect of microRNA-34a in cell cycle, differentiation, and apoptosis: A review

The tumor suppressor gene p53 was shown to directly regulate the expression of microRNA‐34a (miR‐34a). miR‐34a regulates a plethora of target proteins, which are involved in cell cycle, apoptosis, differentiation, and cellular development.miR‐34a resides in the region of chromosome 1p36.23, which is...

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Published inJournal of biochemical and molecular toxicology Vol. 26; no. 2; pp. 79 - 86
Main Authors Chen, Fei, Hu, Shen-Jiang
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.02.2012
Subjects
Animals
Antibody-Dependent Cell Cytotoxicity
Apoptosis
Base Sequence
Cell Cycle
Cell Differentiation
Differentiation
Gene Expression Regulation
Humans
MicroRNAs - genetics
MicroRNAs - metabolism
MicroRNAs - physiology
miR-34a
Molecular Sequence Data
Neoplasms - genetics
Neoplasms - metabolism
RNA Interference
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Summary:The tumor suppressor gene p53 was shown to directly regulate the expression of microRNA‐34a (miR‐34a). miR‐34a regulates a plethora of target proteins, which are involved in cell cycle, apoptosis, differentiation, and cellular development.miR‐34a resides in the region of chromosome 1p36.23, which is commonly deleted in many tumor types, while it results in the loss expression of miR‐34a. The promoters of the miR‐34a gene subject to inactivation by CpG methylation also induce the loss expression of miR‐34a. Ectopic miR‐34a expression induces apoptosis, cell cycle arrest, and differentiation or reduces migration. This review summarizes the progress regarding the role of miR‐34a in cell cycle, differentiation, and apoptosis. © 2011 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:79–86 2012; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.20412
Bibliography:ark:/67375/WNG-4PCZZL9S-M
istex:C7543E284F3EA4A19702C706B28CE58383C13296
ArticleID:JBT20412
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:1095-6670
1099-0461
1099-0461
DOI:10.1002/jbt.20412