Mitochondrial RNA helicase DDX28 promotes cell cycle and DNA repair programs and shapes an immunosuppressive microenvironment in acute myeloid leukemia
A mitochondrial protein linked to poor outcomes in AML may unlock new therapeutic targets at the intersection of cell metabolism and immune suppression.
Integrated bioinformatics analysis across AML cohorts identifies DDX28 (mitochondrial RNA helicase) as a novel prognostic biomarker associated with poor survival and an immunosuppressive tumour microenvironment. In vitro siRNA knockdown confirms a functional role in AML cell proliferation and migration, positioning DDX28 as a candidate therapeutic target linking mitochondrial translation to immune evasion.
What the study was
- Study design
- Multi-omics bioinformatics + in vitro siRNA knockdown
- Population
- AML patients (multiple public cohorts via multi-omics resources); in vitro HEL cell line
- Category
- Diagnostics
- Maturity
- Exploratory
- Journal
- Translational Oncology
Why it surfaced
Novel mitochondrial-immune axis in AML with functional validation; bioinformatics-forward study without clinical cohort; capped at STANDARD per preclinical/computational design
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