Control of stress signaling in stem cells: crossroads of stem cells and cancer

被引:0
作者
Cho, Seung-Ju [1 ]
Koo, JaeHyung [2 ]
Chun, Kwang-Hoon [3 ]
Cha, Hyuk-Jin [1 ]
机构
[1] Sogang Univ, Dept Life Sci, Seoul 04107, South Korea
[2] DGIST, Dept Brain & Cognit Sci, Daegu, South Korea
[3] Gachon Univ, Gachon Inst Pharmaceut Sci, Coll Pharm, Inchon 21936, South Korea
基金
新加坡国家研究基金会;
关键词
Stem cells; Stress modulator; Anti-growth signals; Oncogenic susceptibility; ENDOTHELIAL PROGENITOR CELLS; SELF-RENEWAL; WIP1; PHOSPHATASE; LUNG-CANCER; DNA-DAMAGE; P16(INK4A) INACTIVATION; PROLIFERATIVE CAPACITY; COLORECTAL-CANCER; BMI-1; SENESCENCE;
D O I
10.1007/s13277-016-5249-x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Tumorigenesis is a relatively rare event in the human body considering the enormous number of cells composing our body and the frequent occurrence of genetic mutations in each cell. Nevertheless, the cells that happen to meet the minimum requirements can be transformed when stressed by a variety of oncogenic stimulations, then progress to form tumors. The vigorous competition between oncogenic signaling and tumor-suppressor defense is a critical determinant of cellular fate, which can be either tumorigenic transformation or cellular senescence/apoptosis depending on "who wins the battle." Recently, a number of cancers have been reported to originate from stem cells, whose self-renewing properties are normally reduced by innate tumor suppressors. Therefore, exploring the innate mechanism by which stem cells modulate tumor suppressors to maintain their "stemness" may provide valuable clues to characterize the distinctive oncogenic susceptibility of stem cells. This review is focused on the recent advances in the field of tumorigenesis of stem cells and on the associated molecular mechanisms.
引用
收藏
页码:12983 / 12990
页数:8
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