ACADSB regulates ferroptosis and affects the migration, invasion, and proliferation of colorectal cancer cells

GPX4 脂质过氧化 谷胱甘肽还原酶 谷胱甘肽 癌症研究 谷胱甘肽过氧化物酶 结直肠癌 细胞凋亡 细胞生长 丙二醛 癌细胞 细胞生物学 细胞 生物 癌症 基因敲除 化学 转移 氧化应激 生物化学 遗传学
作者
Di Lu,Zhiyu Yang,Qiaoyun Xia,Shanjun Gao,Suofeng Sun,Xiaoying Luo,Zhen Li,Xiulei Zhang,Xiuling Li
出处
期刊:Cell Biology International [Wiley]
卷期号:44 (11): 2334-2343 被引量:45
标识
DOI:10.1002/cbin.11443
摘要

Abstract Colorectal cancer (CRC) is one of the most pressing health issues in today's society. As such, it is imperative that the scientific community devise effective methods to inhibit the proliferation and metastasis of CRC cells. Ferroptosis is a recently discovered regulatory cell death mode mainly manifested by dysregulation of cellular iron metabolism and mitochondrial lipid peroxidation. ACADSB is a member of the acyl‐CoA dehydrogenase. This study finds that ACADSB is lowly expressed in CRC tissues. Its expression is negatively correlated with N‐ and M‐stage CRC but positively correlated with the overall survival rate of CRC patients. In addition, it finds that ACADSB is found in the mitochondria of cells. Overexpression of ACADSB inhibits CRC cell migration, invasion, and proliferation, while ACADSB knockdown has the opposite effect. More importantly, the study finds that ACADSB negatively regulates expression of glutathione reductase and glutathione peroxidase 4, the two main enzymes responsible for clearing glutathione (GSH) in CRC cells. ACADSB overexpression enhances the concentration of malondialdehyde, Fe + , superoxide dismutase, and lipid peroxidation in CRC cells, but reduces the concentration of GSH. This is significant, as all of these are important indicators of ferroptosis. Evaluating the data as a whole, this paper speculates that ACADSB affects CRC cell migration, invasion, and proliferation by regulating CRC cell ferroptosis.
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