Roles of N6-Methyladenosine Demethylase FTO in Malignant Tumors Progression.
Qing-Kang ZhengChao MaIrfan UllahKang HuRui-Jie MaNan ZhangZhi-Gang SunPublished in: OncoTargets and therapy (2021)
In 2007, the fat mass and obesity-associated (FTO) gene was discovered initially to regulate body mass index and obesity and was subsequently found to be the first mRNA N6-methyladenosine (m6A) demethylation enzyme, which can demethylate m6A. A growing body of evidence shows that m6A modification is involved in a variety of cell biological processes, including cell proliferation, apoptosis, and self-renewal through different regulatory mechanisms. In recent years, a large number of studies have found that m6A modification play key role in the occurrence and development of tumors, such as acute myeloid leukemia, breast cancer, lung cancer, etc. As a function of m6A demethylase, FTO has attracted more and more attention in cancer. There is evidence that specific FTO single nucleotide polymorphisms (SNPs) may be significantly associated with overweight and cancer susceptibility by regulating the expression of related genes. Besides, when the expression level of FTO is altered or dysfunctional, it may be involved in the occurrence and progression of a variety of tumors as a tumor suppressor gene or oncogene, usually in an m6A-dependent manner. Further research found that FTO is involved in the development of different kinds of malignant tumors, but the mechanism is unknown. According to this review, The FTO gene's research progress in tumors is reviewed, aiming to find new targets for molecular pathological diagnosis and molecular targeted therapy of tumors.
Keyphrases
- acute myeloid leukemia
- cell proliferation
- genome wide
- weight loss
- poor prognosis
- metabolic syndrome
- insulin resistance
- type diabetes
- papillary thyroid
- copy number
- risk assessment
- oxidative stress
- weight gain
- cell death
- adipose tissue
- physical activity
- gene expression
- working memory
- stem cells
- squamous cell carcinoma
- cell cycle
- transcription factor
- endoplasmic reticulum stress
- skeletal muscle
- squamous cell
- lymph node metastasis
- acute lymphoblastic leukemia
- cell therapy
- mesenchymal stem cells
- signaling pathway
- cell cycle arrest
- fatty acid
- pi k akt