调节器
甲基化
DNA甲基化
生物
癌症研究
细胞凋亡
N6-甲基腺苷
氧化应激
基因表达调控
基因表达
基因
生物化学
甲基转移酶
作者
Jun Wu,Xiaoqin Wang,Xin Li
出处
期刊:Epigenomics
[Future Medicine]
日期:2022-12-01
卷期号:14 (23): 1509-1522
被引量:2
标识
DOI:10.2217/epi-2022-0403
摘要
Aims: This study aimed to reveal the possible molecular mechanism of n6-methyladenosine (m6A) methylation regulator FTO in the biological activities of ovarian cancer (OC) based on The Cancer Genome Atlas, Genotype-Tissue Expression and Gene Expression Omnibus databases. Materials & methods: A risk score model was constructed to predict the prognosis of patients with OC. The key m6A methylation regulator was screened out based on OC-related microarray datasets. Results: 22 m6A methylation regulators were differentially expressed and interacted with each other in OC. FTO, a key m6A methylation regulator, was singled out. In vivo experiments verified that FTO promoted oxidative stress and apoptosis of OC cells to inhibit tumor growth in nude mice. Conclusion: This study highlighted the tumor-suppressive mechanism of m6A methylation regulator FTO in OC.
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