AI Article Synopsis
- Gastric cancer (GC) ranks as the 5th most common cancer and 4th leading cause of cancer-related deaths worldwide, with FTO identified as a key player in its development due to its role as an m6A demethylase.
- In this study, researchers found that FTO levels are significantly higher in GC tissues and cells, correlating with more severe disease characteristics and worse patient outcomes.
- The study reveals that FTO enhances GC cell growth and movement by affecting specific proteins in a signaling pathway, suggesting its potential as a biomarker for diagnosing and predicting treatment responses in GC patients.
Article Abstract
Gastric cancer (GC) is the 5 most prevalent cancer and the 4 primary cancer-associated mortality globally. As the first identified m6A demethylase for removing RNA methylation modification, fat mass and obesity-associated protein (FTO) plays instrumental roles in cancer development. Therefore, we study the biological functions and oncogenic mechanisms of FTO in GC tumorigenesis and progression. In our study, FTO expression is obviously upregulated in GC tissues and cells. The upregulation of FTO is associated with advanced nerve invasion, tumor size, and LNM, as well as the poor prognosis in GC patients, and promoted GC cell viability, colony formation, migration and invasion. Mechanistically, FTO targeted specificity protein 1 and Aurora Kinase B, resulting in the phosphorylation of ataxia telangiectasia mutated and P38 and dephosphorylation of P53. In conclusion, the m6A demethylase FTO promotes GC tumorigenesis and progression by regulating the SP1-AURKB-ATM pathway, which may highlight the potential of FTO as a diagnostic biomarker for GC patients' therapy response and prognosis.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11220007 | PMC |
| http://dx.doi.org/10.1038/s42003-024-06477-y | DOI Listing |
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