Observational analysis reveals METTL14's impact on imatinib resistance in chronic myeloid leukemia, suggesting a role in apoptosis regulation.
Key Points
METTL14 expression is significantly elevated in imatinib-resistant CML patients and cell lines, highlighting its potential role in leukemia progression.
Overexpression of METTL14 promotes cell proliferation, inhibits apoptosis, and increases drug resistance in chronic myeloid leukemia cells.
Mechanistically, METTL14 affects Bcl-x splicing, which disrupts the apoptosis pathway, indicating its crucial role in CML biology.
Silencing METTL14 reduces m6A levels and enhances apoptosis, further suggesting its significance in therapeutic resistance.