OncoTargets and Therapy (Sep 2021)
Roles of N6‐Methyladenosine Demethylase FTO in Malignant Tumors Progression
Abstract
Qing-Kang Zheng,1 Chao Ma,1 Irfan ullah,2 Kang Hu,1 Rui-Jie Ma,3 Nan Zhang,4 Zhi-Gang Sun5 1School of Clinical Medicine, Weifang Medical University, Weifang, People’s Republic of China; 2Department of Surgery, Khyber Medical University Peshawar, Peshawar, Pakistan; 3Cheeloo College of Medicine, Shandong University, Jinan, People’s Republic of China; 4Department of Oncology, Central Hospital Affiliated to Shandong First Medical University, Jinan, People’s Republic of China; 5Department of Thoracic Surgery, Central Hospital Affiliated to Shandong First Medical University, Jinan, People’s Republic of ChinaCorrespondence: Zhi-Gang SunDepartment of Thoracic Surgery, Central Hospital Affiliated to Shandong First Medical University, Jinan, 250013, People’s Republic of ChinaTel +8613370582825Email [email protected] ZhangDepartment of Oncology, Central Hospital Affiliated to Shandong First Medical University, Jinan, 250013, People’s Republic of ChinaTel +8613370582850Email [email protected]: 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.Keywords: FTO, cancers, N6-methyladenosine, SNPs, FTO inhibitors
