Dynamics of ARF regulation that control senescence and cancer

ARF is an alternative reading frame product of the INK4a/ARF locus, inactivated in numerous human cancers. ARF is a key regulator of cellular senescence, an irreversible cell growth arrest that suppresses tumor cell growth. It functions by sequestering MDM2 (a p53 E3 ligase) in the nucleolus, thus a...

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Bibliographic Details
Published inBMB reports Vol. 49; no. 11; pp. 598 - 606
Main Authors Ko, Aram, Han, Su Yeon, Song, Jaewhan
Format Journal Article
LanguageKorean
Published 생화학분자생물학회 30.11.2016
Subjects
ARF
ARF knockout mice
Cancer
Posttranslational reg-ulation
Senescence
Tumorigenesis
Ubiquitination
ARF knockout mice
Senescence
Ubiquitination
ARF
Tumorigenesis
Posttranslational regulation
Cancer
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Summary:ARF is an alternative reading frame product of the INK4a/ARF locus, inactivated in numerous human cancers. ARF is a key regulator of cellular senescence, an irreversible cell growth arrest that suppresses tumor cell growth. It functions by sequestering MDM2 (a p53 E3 ligase) in the nucleolus, thus activating p53. Besides MDM2, ARF has numerous other interacting partners that induce either cellular senescence or apoptosis in a p53-independent manner. This further complicates the dynamics of the ARF network. Expression of ARF is frequently disrupted in human cancers, mainly due to epigenetic and transcriptional regulation. Vigorous studies on various transcription factors that either positively or negatively regulate ARF transcription have been carried out. However, recent focus on posttranslational modifications, particularly ubiquitination, indicates wider dynamic controls of ARF than previously known. In this review, we discuss the role and dynamic regulation of ARF in senescence and cancer. [BMB Reports 2016; 49(11): 598-606]
Bibliography:Korean Society for Biochemistry and Molecular Biology
KISTI1.1003/JNL.JAKO201606776011005
ISSN:1976-6696
1976-670X