ArticleOncogene2026
LncRMRP drives bladder cancer invasion via a lactylation-driven positive feedback circuit.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
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Authors and funding
12 authors.
Funding
Abstract
Muscle-invasive bladder cancer (MIBC) remains highly aggressive. We identified the long non-coding RNA RMRP as significantly upregulated in MIBC. Functional studies demonstrated that RMRP promotes invasive phenotypes and glycolytic reprogramming. Mechanistically, RMRP binds pyruvate dehydrogenase complex X component (PDHX) and weakens the PDHX-dihydrolipoamide dehydrogenase (DLD) interaction, thereby impairing pyruvate dehydrogenase complex (PDC) function, reducing pyruvate dehydrogenase (PDH) activity, and shifting pyruvate metabolism toward lactate production. The resulting lactate promotes p300-dependent lactylation of insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) at K272 and K561, thereby stabilizing IGF2BP1 by reducing ubiquitin-mediated degradation. Stabilized IGF2BP1, in turn, binds to RMRP and stabilizes it. This establishes an RMRP-PDHX-lactate-IGF2BP1 positive feedback loop that continuously amplifies the invasive phenotype of MIBC. These findings reveal a novel mechanism by which RMRP promotes invasion through metabolic reprogramming and lactylation-mediated feedback, highlighting a potential therapeutic target for MIBC.
Identifiers
42533112What Socratic 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 Socratic graph.