N6-甲基腺苷（m6A）在各种癌症的发生和发展中起到关键作用。脂肪量和肥胖相关蛋白（FTO）由于其去甲基酶活性而参与多种癌症，并且FTO促进膀胱癌增殖和迁移的分子机制仍需进一步研究。本研究中，发现FTO在膀胱癌中上调，并与不良预后有关。通过增加和减少功能实验表明，FTO的上调促进了膀胱癌的增殖和迁移。机制研究显示，FTO以m6A依赖的方式增强了信号转导子和转录激活因子3（STAT3）mRNA的稳定性，从而增加了STAT3的表达，随后促进了P-STAT3的表达和激活STAT3信号通路。总体而言，本研究揭示了FTO在膀胱癌进展中的关键作用，并为调控癌基因STAT3提供了新的途径。

N6-Methyladenosine (m6A) plays a key role in the occurrence and development of various cancers. Fat mass and obesity-associated protein (FTO) was is involved in multiple cancers owing to its demethylase activity, and the molecular mechanism underlying FTO-promoted bladder cancer proliferation and migration via the regulation of RNA stability requires further investigation. In the present study, FTO was upregulated in bladder cancer and related to poor prognosis. Gain- and loss-of-function experiments showed that the upregulation of FTO promoted bladder cancer proliferation and migration. Mechanistic studies showed that FTO enhanced the stability of signal transducer and activator of transcription 3 (STAT3) mRNA in an m6A-dependent manner, thereby increasing STAT3 expression, which subsequently promoted P-STAT3 expression and activated STAT3 signalling pathway. Overall, this study revealed that the critical role of FTO in the progression of bladder cancer and could provide a novel avenue to regulate oncogene STAT3.