Role of Oxidative Stress in Stem, Cancer, and Cancer Stem Cells

作者
Ahmed Abdal Dayem,Hye-Yeon Choi,Jung‐Hyun Kim,Ssang‐Goo Cho
出处
期刊:Cancers [Multidisciplinary Digital Publishing Institute]
卷期号:2 (2): 859-884 被引量:232
标识
DOI:10.3390/cancers2020859
摘要

The term ''oxidative stress" refers to a cell's state characterized by excessive production of reactive oxygen species (ROS) and oxidative stress is one of the most important regulatory mechanisms for stem, cancer, and cancer stem cells. The concept of cancer stem cells arose from observations of similarities between the self-renewal mechanism of stem cells and that of cancer stem cells, but compared to normal stem cells, they are believed to have no control over the cell number. ROS have been implicated in diverse processes in various cancers, and generally the increase of ROS in cancer cells is known to play an important role in the initiation and progression of cancer. Additionally, ROS have been considered as the most significant mutagens in stem cells; when elevated, blocking self-renewal and at the same time, serving as a signal stimulating stem cell differentiation. Several signaling pathways enhanced by oxidative stress are suggested to have important roles in tumorigenesis of cancer or cancer stem cells and the self-renewal ability of stem or cancer stem cells. It is now well established that mitochondria play a prominent role in apoptosis and increasing evidence supports that apoptosis and autophagy are physiological phenomena closely linked with oxidative stress. This review elucidates the effect and the mechanism of the oxidative stress on the regulation of stem, cancer, and cancer stem cells and focuses on the cell signaling cascades stimulated by oxidative stress and their mechanism in cancer stem cell formation, as very little is known about the redox status in cancer stem cells. Moreover, we explain the link between ROS and both of apoptosis and autophagy and the impact on cancer development and treatment. Better understanding of this intricate link may shed light on mechanisms that lead to better modes of cancer treatment.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
0411345完成签到,获得积分10
刚刚
刚刚
搜集达人应助包容老黑采纳,获得10
刚刚
huihui发布了新的文献求助10
刚刚
刚刚
科研通AI6.4应助ssslllppp采纳,获得10
刚刚
1秒前
bkagyin应助Waverly采纳,获得10
2秒前
2秒前
科研通AI6.4应助Leo采纳,获得10
2秒前
jojo发布了新的文献求助10
3秒前
XNM发布了新的文献求助10
3秒前
大刘发布了新的文献求助10
4秒前
Aisha完成签到,获得积分10
4秒前
mortal完成签到,获得积分10
4秒前
5秒前
Dog发布了新的文献求助10
5秒前
6秒前
6秒前
秋山澪发布了新的文献求助10
6秒前
李健的粉丝团团长应助iu采纳,获得10
6秒前
7秒前
7秒前
科研通AI6.4应助liu采纳,获得10
7秒前
sanlang完成签到,获得积分10
7秒前
直率一手发布了新的文献求助10
9秒前
科研通AI6.4应助dde采纳,获得10
9秒前
天天快乐应助dde采纳,获得10
9秒前
Nole应助葵葵采纳,获得10
9秒前
科研通AI6.4应助dde采纳,获得10
9秒前
huihui完成签到,获得积分10
9秒前
ivanka完成签到,获得积分10
10秒前
宇宙无敌超人完成签到,获得积分10
10秒前
cdercder应助Aisha采纳,获得20
10秒前
10秒前
dde应助elastos采纳,获得10
11秒前
万能图书馆应助橙橙采纳,获得10
11秒前
传奇3应助RRR采纳,获得10
12秒前
万事无忧发布了新的文献求助10
12秒前
单薄的友灵完成签到,获得积分10
13秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
China Pluperfect I: Epistemology of Past and Outside in Chinese Art 520
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
Governing Growth: Us Industrial Policy from Hamilton to Trump 500
The fast track to determining transfer functions of linear circuits: The student guide 500
The Analytical and Numerical Solution of Electric and Magnetic Fields 500
Synthesis of P-Chiral Phosphine Ligands and Their Applications in Asymmetric Catalysis 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7624816
求助须知:如何正确求助?哪些是违规求助? 9199792
关于积分的说明 19723958
捐赠科研通 7195761
什么是DOI,文献DOI怎么找? 3273562
关于科研通互助平台的介绍 2435737
邀请新用户注册赠送积分活动 2269423