ArticleCell death and differentiation2026
PSMD14-mediated PFKFB2 deubiquitination activates H3K27 lactylation to drive cancer stemness in gastric adenocarcinoma.
Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- Lactate metabolism and protein lactylation in inflammatory and tumor microenvironments.Molecular biomedicine · 2026Review
- Unveiling Lactylation: A Novel Frontier in Cancer Stemness and Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Orchestrating glucose metabolism: PFKFB2 as a signal-integrating conductor in homeostasis and disease.The Journal of biological chemistry · 2026Review
- Crosstalk between lactylation and other post-translational modifications in health and diseases.Molecular biomedicine · 2026Review
- Ubiquitination and NOncology letters · 2026Review
- PSMD14 as a translational target in cancer and beyond: from deubiquitination mechanisms to drug resistance and precision therapy.Cancer drug resistance (Alhambra, Calif.) · 2026Review
- Targeting Lactylation for Cancer: Mechanisms, Effects, and Therapeutic Prospects.International journal of molecular sciences · 2025Review
- Post-translational modifications in hepatocellular carcinoma: mechanisms and therapeutic potential.Medical oncology (Northwood, London, England) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
Deubiquitinases (DUBs) are pivotal in cancer progression, yet their role in metabolic reprogramming in gastric adenocarcinoma (GAC) remains unclear. Here, we discover that highly expressed PSMD14 strengthens tumor stemness and drives tumor progression by increasing glycolysis and lactate accumulation, which activates H3K27 lactylation (H3K27la) and turns to enhance the expression of PSMD14 and SOX9. Mechanistically, PSMD14 deubiquitinates PFKFB2 at K355, facilitating SCYL2-mediated phosphorylation of PFKFB2 at S466/S483, which increases the generation of fructose-2,6-bisphosphate, activating PFK1 and glycolysis. Additionally, the H3K27la/PSMD14/SCYL2/p-PFKFB2 axis correlates with increased glucose metabolic activity and poor prognosis in GAC patients. Notably, high-throughput screening of FDA-approved drugs reveals that Daclatasvir (DCV) exhibits high binding affinity for PSMD14 protein, disrupts the PSMD14-PFKFB2 interaction, reduces PFKFB2 activity and tumor burden. Collectively, our findings are the first to elucidate a positive feedback loop existing between PSMD14 and glycolysis in GAC progression, suggesting that PSMD14 blockade may represent a potential therapeutic approach for GAC.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.