FTO (Alpha-Ketoglutarate-Dependent Dioxygenase FTO)

Clinically, ROLLCSC and its targets are associated with distinct tumor expression patterns and have prognostic significance. Overall, our study elucidates how the lncRNA ROLLCSC derived from cancer stem cell (CSC)-derived EVs is efficiently transported to LUAD cells, subsequently reshaping the lipid metabolism of recipient cells and enhancing their resistance to ferroptosis.

Furthermore, we detail a diagnostic-therapeutic roadmap that integrates liquid biopsy-based m6A biomarker detection with subtype-specific treatment assignment. Targeting the m6A epitranscriptome represents a paradigm shift in oncology; our framework provides the essential strategic approach needed to overcome context-dependency, offering a logical structure for tumor classification, vulnerability prediction, and the translation of epitranscriptomic insights into patient benefit through personalized, biomarker-guided combination therapies.

In addition, the products exhibit a significantly limited movement within the enclosed intracellular milieu, which makes this system particularly suitable for truly in situ visualization of FTO and the observation of its demethylation in living cells. Moreover, our strategy can accurately evaluate the repair activity of FTO after various drug treatments and differentiate cancer cells from normal ones according to the expression level of FTO, providing a simple but reliable tool for clinical diagnosis and drug discovery.

Morbid obesity is characterized by a pro-inflammatory and metabolically adverse molecular signature reflected in accelerated glycomic aging. Personalized nutrigenetic dietary interventions, derived from AI-driven analysis of whole-genome sequencing (WGS) data, effectively reduced both BMI and biological age markers, supporting integrative multi-omics and machine learning approaches as promising tools in precision-based obesity management.

Recurrent insertions were located near cancer-associated genes, including RB1, NEDD4, FTO, LAMA2, NOD1, and KCNB2, implicating LINE-1 activity in cis-regulatory remodeling of oncogenic pathways. Together, these findings indicate that LINE-1 transcript heterogeneity in NSCLC is shaped by host genomic architecture and conserved functional hotspots, providing new insights into the mechanisms of genetic and epigenetic dysregulation associated with LINE-1 retroelements.

FTO significantly influences cervical cancer progression, at least in part, through m6A modification of FGF2, thereby affecting downstream signaling. Targeting FTO and its downstream effectors holds potential as a therapeutic strategy for cervical cancer treatment.

Functionally, YTHDF2 promoted malignant phenotypes in keratinocytes and exacerbated arsenic-induced skin lesions in mice, accompanied by activation of the PRR5-mTORC2-AKT axis and enhancement SMAD2/3 signaling. This study advances our understanding of how opposing m6A regulatory axes shape YTHDF2 engagement and mRNA decay outputs, thereby promoting arsenic carcinogenesis by regulating oncogenic and tumor-suppressive signaling.

Preclinical studies show that genetic depletion, small-molecule inhibition, or targeted degradation of FTO increases m6A on key targets, suppresses leukemic growth, and can sensitize cells to standard therapies, supporting FTO as a druggable epitranscriptomic vulnerability. This review summarizes FTO structure and function, highlights subtype-specific mechanisms in AML and ALL, and discusses emerging therapeutic strategies and translational challenges.

The relationship between SERPINF1 and FTO was determined through correlation analysis, methylated RNA immunoprecipitation, luciferase, RT-qPCR, Western blotting, RNA immunoprecipitation, and actinomycin D treatment assays...Rescue experiments demonstrated that SERPINF1 overexpression reversed FTO-induced oncogenic phenotypes. These findings suggest that FTO-mediated m6A demethylation suppressed SERPINF1 expression in MM, whereas SERPINF1 overexpression inhibited tumor progression via the Wnt/β-catenin pathway.

In vivo studies in tumor-bearing mice demonstrated specific tumor accumulation, precise signal localization, and minimal systemic toxicity. This work establishes a sensitive, specific, and biocompatible platform for multiplexed visualization of demethylase activities in living cells and animals, providing a valuable tool for understanding cancer epigenetics and guiding targeted therapeutic development.

Clinically approved drugs such as Dasatinib (targeting CSK) and Crizotinib (targeting MET) emerged as promising candidates due to favorable pharmacokinetics and known bioactivity. Host-directed therapeutics could offer alternative strategies to conventional antibiotic therapy, addressing challenges such as resistance and infection recurrence, providing a foundation for future experimental validation and development of host-targeted interventions for infection control.

Moreover, new therapies, like small-molecule inhibitors aimed at enzymes such as METTL3 and FTO that play important roles in m6A are introduced in this review, which could aid in eradicating LCSCs and overcoming treatment failure. m6A pathway is a promising target for discovering new therapies to combat the recurrence of lung cancer.