Nucleotide metabolism, oncogene-induced senescence and cancer

被引：131

作者：

Aird, Katherine M. ^{[1
]}

Zhang, Rugang ^{[1
]}

机构：

[1] Wistar Inst Anat & Biol, Ctr Canc, Gene Express & Regulat Program, Philadelphia, PA 19104 USA

来源：

CANCER LETTERS | 2015年 / 356卷 / 02期

关键词：

Nucleotide metabolism; Cancer; Oncogene-induced senescence; DNA damage response; Replication stress; Cancer therapy; RIBONUCLEOTIDE REDUCTASE INHIBITORS; DNA-REPLICATION STRESS; 3-AMINOPYRIDINE-2-CARBOXALDEHYDE THIOSEMICARBAZONE 3-AP; THYMIDYLATE SYNTHASE; PROGNOSTIC BIOMARKER; CELL SENESCENCE; PHASE-I/II; EXPRESSION; DAMAGE; P53R2;

D O I：

10.1016/j.canlet.2014.01.017

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Senescence is defined as a stable cell growth arrest. Oncogene-induced senescence (OIS) occurs when an activated oncogene is expressed in a normal cell. OIS acts as a bona fide tumor suppressor mechanism by driving stable growth arrest of cancer progenitor cells harboring the initial oncogenic hit. OIS is often characterized by aberrant DNA replication and the associated DNA damage response. Nucleotides, in particular deoxyribonucleotide triphosphates (dNTPs), are necessary for both DNA replication and repair. Imbalanced dNTP pools play a role in a number of human diseases, including during the early stages of cancer development. This review will highlight what is currently known about the role of decreased nucleotide metabolism in OIS, how nucleotide metabolism leads to transformation and tumor progression, and how this pathway can be targeted as a cancer therapeutic by inducing senescence of cancer cells. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

引用

页码：204 / 210

页数：7

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