线粒体分裂
结直肠癌
线粒体融合
癌症研究
MFN1型
生物
线粒体
大肠癌小鼠模型的建立
细胞凋亡
癌症
重编程
血管生成
细胞生物学
生物信息学
线粒体DNA
细胞
遗传学
基因
作者
Zihong Wu,Chong Xiao,Fang Li,Wenbo Huang,Fengming You,Xueke Li
标识
DOI:10.1002/1878-0261.13578
摘要
The incidence and mortality rates of colorectal cancer have elevated its status as a significant public health concern. Recent research has elucidated the crucial role of mitochondrial fusion–fission dynamics in the initiation and progression of colorectal cancer. Elevated mitochondrial fission or fusion activity can contribute to the metabolic reprogramming of tumor cells, thereby activating oncogenic pathways that drive cell proliferation, invasion, migration, and drug resistance. Nevertheless, excessive mitochondrial fission can induce apoptosis, whereas moderate mitochondrial fusion can protect cells from oxidative stress. This imbalance in mitochondrial dynamics can exert dual roles as both promoters and inhibitors of colorectal cancer progression. This review provides an in‐depth analysis of the fusion–fission dynamics and the underlying pathological mechanisms in colorectal cancer cells. Additionally, it offers partial insights into the mitochondrial kinetics in colorectal cancer‐associated cells, such as immune and endothelial cells. This review is aimed at identifying key molecular events involved in colorectal cancer progression and highlighting the potential of mitochondrial dynamic proteins as emerging targets for pharmacological intervention.
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