自噬
细胞生物学
粒体自噬
下调和上调
生物
癌细胞
PI3K/AKT/mTOR通路
细胞
小RNA
癌症研究
信号转导
细胞凋亡
癌症
基因
遗传学
作者
Basheer Abdullah Marzoog,Т. И. Власова
出处
期刊:Current Cancer Drug Targets
[Bentham Science]
日期:2022-08-26
卷期号:22 (9): 749-756
被引量:1
标识
DOI:10.2174/1568009622666220428102741
摘要
Basal autophagy plays a crucial role in maintaining intracellular homeostasis and prevents the cell from escaping the cell cycle regulation mechanisms and being cancerous. Mitophagy and nucleophagy are essential for cell health. Autophagy plays a pivotal role in cancer cell transformation, where upregulated precancerous autophagy induces apoptosis. Impaired autophagy has been shown to upregulate cancer cell transformation. However, tumor cells upregulate autophagy to escape elimination and survive the unfavorable conditions and resistance to chemotherapy. Cancer cells promote autophagy through modulation of autophagy regulation mechanisms and increase expression of the autophagyrelated genes. Whereas, autophagy regulation mechanisms involved microRNAs, transcription factors, and the internalized signaling pathways such as AMPK, mTOR, III PI3K, and ULK-1. Disrupted regulatory mechanisms are various as the cancer cell polymorphism. Targeting a higher level of autophagy regulation is more effective, such as gene expression, transcription factors, or epigenetic modification that are responsible for the up-regulation of autophagy in cancer cells. Currently, the CRISPR-CAS9 technique is available and can be applied to demonstrate the potential effects of autophagy in cancerous cells.
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