MicroRNA miR‐24 promotes cell proliferation by targeting the CDKs inhibitors p27Kip1 and p16INK4a. Issue 10 (20th June 2013)

• Record Type: Journal Article
• Authors: Giglio, Simona; Cirombella, Roberto; Amodeo, Rachele; Portaro, Luciano; Lavra, Luca; Vecchione, Andrea
• Is Part Of: Journal of cellular physiology. Volume 228:Issue 10(2013:Oct.)
• Page Start: 2015
• Page End: 2023
• Publication Date: 2013-06-20
• Subjects: Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.24368
• Languages: English
• ISSNs: 0021-9541

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="jcp24368-sec-0001" sec-type="section"> <p>Cell cycle progression is controlled by numerous mechanisms ensuring correct cell division. The transition from one cell cycle phase to another occurs in an orderly fashion and is regulated by different cellular proteins. Therefore an alteration of the regulatory mechanisms of the cell cycle results in uncontrolled cell proliferation, which is a distinctive feature of human cancers. Recent evidences suggest that microRNAs (miRs) may also control the levels of multiple cell cycle regulators and therefore control cell proliferation. In fact miRs are a class of small non‐coding RNAs, which modulate gene expression. They are involved in numerous physiological cellular processes and most importantly accumulating evidence indicates that many miRs are aberrantly expressed in human cancers. In this report we describe that miR‐24 directly targets p27^Kip1 and p16^Ink4a in primary keratinocyte and in different cancer derived cell lines promoting their proliferation, suggesting that miR‐24 is involved in cyclin‐dependent kinase inhibitors post‐transcriptional regulation and that upregulation of miR‐24 may play a role in carcinogenesis. J. Cell. Physiol. 228: 2015–2023, 2013. © 2013 Wiley Periodicals, Inc.</p> </sec> </abstract>