Abstract: Fat mass and obesity-associated protein （FTO）, the first identified obesity-susceptibility gene, exerts complex roles in tumors via its RNA demethylase function. Through modulation of N6-methyladenosine （m⁶A） modification levels on mRNA, FTO influences the stability of oncogenes and related signaling pathways, thereby promoting metabolic reprogramming, proliferation, invasion, and chemoresistance in tumor cells. In obesity-related tumors, FTO expression exhibits tissue-specific patterns： it is highly expressed in endometrial, colorectal, pancreatic and breast cancers, where it facilitates tumor progression by activating an immunosuppressive microenvironment and glycolysis. Conversely, FTO expression is downregulated in thyroid cancer, inhibiting malignancy through the regulation of ferroptosis. Additionally, FTO exerts dual oncogenic or tumor-suppressive roles in ovarian and liver cancers, depending on molecular contexts and subtypes. FTO expression correlates closely with tumor staging, metastasis, and prognosis, underscoring its potential as a novel prognostic biomarker. Small-molecule inhibitors targeting FTO have demonstrated promising antitumor effects in preclinical models, presenting a new therapeutic strategy for precision intervention in obesity-associated cancers. This review summarizes the molecular mechanisms and translational prospects of FTO in obesity-related tumors, providing theoretical support for precision medical strategies.