Abstract: 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


中文翻译：

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N6-甲基腺苷脱甲基酶FTO在恶性肿瘤进展中的作用

摘要：2007 年，脂肪量和肥胖相关 (FTO) 基因最初被发现可以调节体重指数和肥胖，随后被发现是第一个 mRNA N6-甲基腺苷 (m6A) 去甲基化酶，可以使 m6A 去甲基化。越来越多的证据表明，m6A 修饰涉及多种细胞生物学过程，包括细胞增殖、凋亡和通过不同调节机制的自我更新。近年来，大量研究发现m6A修饰在肿瘤的发生发展中起关键作用，如急性髓系白血病、乳腺癌、肺癌等。FTO作为m6A去甲基化酶的作用吸引了更多以及对癌症的更多关注。有证据表明，特定的 FTO 单核苷酸多态性 (SNP) 可能通过调节相关基因的表达与超重和癌症易感性显着相关。此外，当FTO的表达水平发生改变或功能失调时，它可能作为抑癌基因或癌基因参与多种肿瘤的发生和发展，通常以m6A依赖性方式参与。进一步研究发现FTO参与了多种恶性肿瘤的发生发展，但其机制尚不清楚。本文综述了FTO基因在肿瘤中的研究进展，旨在为肿瘤的分子病理诊断和分子靶向治疗寻找新的靶点。当FTO的表达水平发生改变或功能失调时，它可能作为抑癌基因或癌基因参与多种肿瘤的发生和发展，通常以m6A依赖性方式参与。进一步研究发现FTO参与了多种恶性肿瘤的发生发展，但其机制尚不清楚。本文综述了FTO基因在肿瘤中的研究进展，旨在为肿瘤的分子病理诊断和分子靶向治疗寻找新的靶点。当FTO的表达水平发生改变或功能失调时，它可能作为抑癌基因或癌基因参与多种肿瘤的发生和发展，通常以m6A依赖性方式参与。进一步研究发现FTO参与了多种恶性肿瘤的发生发展，但其机制尚不清楚。本文综述了FTO基因在肿瘤中的研究进展，旨在为肿瘤的分子病理诊断和分子靶向治疗寻找新的靶点。

关键词： FTO，癌症，N6-甲基腺苷，SNP，FTO抑制剂