ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Hepatocyte BPGM Induces RET Lactylation and Macrophage Reprogramming to Promote Tumorigenesis in Hepatocellular Carcinoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Metabolic Signaling Meets Epigenetic Regulation: How Protein Lactylation Remodels the Tumor Immune Microenvironment in Gastric Cancer.Current issues in molecular biology · 2026Review
- A lactylation- and autophagy-associated prognostic signature reveals LSEC-derived CLEC3B as a novel mediator of hepatocellular carcinoma suppression.PLoS computational biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Aerobic glycolysis is a hallmark of cancer, yet the role of the key glycolytic enzyme bisphosphoglycerate mutase (BPGM) in hepatocellular carcinoma (HCC) progression remains unclear. Here, clinical sample analyses revealed that BPGM expression was upregulated in HCC tissues and associated with poor prognosis. Hepatocyte-specific Bpgm knockout significantly attenuated DEN-induced HCC development in mice. Spatial transcriptomics and single-cell RNA sequencing revealed that hepatocyte-specific Bpgm knockout reduced the monocyte/macrophage infiltration and decreased M2 polarization of tumor-associated macrophages. Additionally, BPGM overexpression promoted the proliferation and migration of HCC cells and enhanced intracellular lactate accumulation. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) identified ret proto-oncogene (RET) as a downstream effector that mediated the effects of BPGM on HCC cells. BPGM promoted P300-mediated lactylation of RET at lysine 549 (K549), which competitively inhibited its ubiquitination, thereby preventing RET protein degradation and enhancing its stability. BPGM in HCC cells also induced both histone lactylation and M2 polarization of macrophages by lactate secretion. This study revealed that BPGM in hepatocytes could enhance RET expression via increasing its lactylation in malignant cells and promote M2 polarization of macrophages, both of which contributed to HCC progression. These findings established that BPGM could act as a potential therapeutic target for HCC.
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.