ArticleMolecular medicine (Cambridge, Mass.)2025
LRP11 facilitates lipid metabolism and malignancy in hepatocellular carcinoma by stabilizing RACK1 through USP5 regulation.
Article in Molecular medicine (Cambridge, Mass.), 2025. 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.
- Review
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- TTC26 scaffolds MINDY3-mediated RACK1 deubiquitination to drive osteoclastogenesis and pathological bone resorption.Journal of orthopaedic translation · 2026Article
- Proteomic analysis identifies lipoprotein(a)-associated proteins linked to incident atherosclerotic cardiovascular disease events.medRxiv : the preprint server for health sciences · 2025Article
- Molecular Network Analysis of HBV Persistent Infection from the Perspective of Whole Transcriptome.Biomolecules · 2025Article
- Stabilization of FASN by USP5-mediated deubiquitination promotes hepatocellular carcinoma progression.Oncogenesis · 2025Article
- LRP11 as a potential predictor of poor prognosis and immune suppression in lung adenocarcinoma.Discover oncology · 2025Article
- Molecular network of metabolic reprogramming and precision diagnosis and treatment of hepatocellular carcinoma.Biomarker research · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Hepatocellular carcinoma (HCC) is one of the most prevalent cancers worldwide and a major public health challenge. Lipid metabolism plays a crucial role in the metabolic reprogramming observed in HCC, although the underlying mechanisms are still being elucidated. Nile red staining and lipid assays showed that LRP11 knockdown significantly reduces lipid accumulation in HCC cells, with a concurrent decrease in key lipid metabolism markers such as FSAN, ACLY and ACSL4, as demonstrated by Western blotting. Mass spectrometry (MS) and co-immunoprecipitation (Co-IP) revealed that LRP11 recruits USP5, enhancing USP5-mediated deubiquitination of RACK1. Truncation analysis identified LRP11 residues 309-500 as critical for interaction with the RACK1 residues 91-231. These findings suggest that LRP11 may influence lipid metabolism and progression in HCC through USP5-mediated stabilization of RACK1. Based on these results, LRP11 emerges as a potential target for further exploration in HCC therapy. Targeting LRP11 or disrupting its interactions with USP5 or RACK1 could offer new avenues for treatment, though additional research is required to validate these therapeutic possibilities.
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