ArticleHaematologica2026
NKX2-1 regulates cell survival, maturation, and DNAdamage responses as a cofactor of RUNX1 in T-cell acute lymphoblastic leukemia.
Article in Haematologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is characterized by ectopic expression of transcription factors, including NKX2- 1, which is over-expressed in 5% of patients. NKX2-1 is associated with a cortical immunophenotype and drives metabolic addiction to the serine/glycine synthesis pathway in T-ALL. However, there is still no complete picture of the role of NKX2- 1 in T-ALL pathogenesis. We characterized a CRISPR-Cas9 NKX2-1 knockout model of RPMI-8402, the only known T-ALL cell line expressing NKX2-1, and validated the obtained results in patient samples. NKX2-1 knockout caused a less mature immunophenotype and promoted cell cycle progression, in line with the direct transcriptional repression of CDK6 by NKX2-1 that we observed. Furthermore, NKX2-1 protected T-ALL cells from apoptosis and DNA damage. The NKX2-1 protein directly bound DNA repair factors, such as RPA1 and RPA2, and presence of NKX2-1 resulted in differential expression of gene sets related to the repair of DNA damage in RPMI-8402 cells and patient samples. Furthermore, NKX2-1 positive cells showed less induction of DNA damage and apoptosis upon treatment with etoposide, a chemotherapy agent that causes DNA damage that is clinically used to treat T-ALL. Mechanistically, our data supported the hypothesis that RUNX1 is an important co-factor for NKX2-1 transcriptional regulation in T-ALL cells, and that NKX2-1 modulated the composition of RUNX1 protein complexes. Notably, NKX2-1 expressing cells showed higher sensitivity towards RUNX1 inhibition, suggesting a co-operative role in regulating T-ALL cell survival. This work reveals a critical role of NKX2-1 in enhancing T-ALL cell survival by protecting against DNA damage and identifies RUNX1 as an important co-factor in T-ALL pathogenesis.
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