ArticleHaematologica2026
The STAT3-VDAC1 axis modulates mitochondrial function and plays a critical role in the survival of acute myeloid leukemia cells.
Article in Haematologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- STAT3 signaling inhibitors for cancer treatment.Trends in pharmacological sciences · 2026Review
- STAT Signaling in Metabolic Disorders: From Molecular Mechanisms to Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- HDAC8 inhibition targets STAT3-MYC axis and synergizes with Venetoclax in KMT2A-rearranged acute myeloid leukemia.Leukemia · 2026Article
- Beating the STATs: targeting the metabolome in acute myeloid leukemia.Haematologica · 2026Article
- Liposomal mitoxantrone, venetoclax and azacitidine in relapsed/refractory acute myeloid leukaemia and early induction failure: a single-centre real-world study.Frontiers in oncology · 2026Article
- Unraveling quantitative trait loci (QTL) overlapping epigenomic regulatory regions associated with feeding behavior in pigs.Frontiers in genetics · 2026Article
- A mitochondrial regulatory network of ferroptosis defense in HPV-positive cervical cancer: therapeutic implications of the mitoSTAT3-DHODH axis.Frontiers in pharmacology · 2026Review
- The ubiquitin-specific protease 21 is critical for cancer cell mitochondrial function and regulates proliferation and migration.The Journal of biological chemistry · 2024Article
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Authors and funding
14 authors.
Funding
Abstract
Signal transducer and activator of transcription 3 (STAT3) is a well-described transcription factor that mediates oxidative phosphorylation and glutamine uptake in bulk acute myeloid leukemia cells and leukemic stem cells. STAT3 has also been shown to translocate to the mitochondria in acute myeloid leukemia cells, and phosphorylation at the serine 727 (pSTAT3 S727) residue has been shown to be especially important for the mitochondrial functions of STAT3. We demonstrate that inhibition of STAT3 results in impaired mitochondrial function and decreased leukemia cell viability. We discovered a novel interaction of STAT3 with voltage-dependent anion channel 1 (VDAC1) in the mitochondria which provides a mechanism through which STAT3 modulates mitochondrial function and cell survival. Through VDAC1, STAT3 regulates calcium and oxidative phosphorylation in the mitochondria. STAT3 and VDAC1 inhibition also results in significantly reduced engraftment potential of leukemia stem cells, including primary samples resistant to venetoclax. These results implicate STAT3 as a therapeutic target in acute myeloid leukemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.