ArticleCommunications biology2024
CAF-EVs carry lncRNA MAPKAPK5-AS1 into hepatocellular carcinoma cells and promote malignant cell proliferation.
Article in Communications biology, 2024. 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
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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.
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Who cites it
2 citing papers in PubMed.
- Pleiotropic mechanisms of cancer-associated fibroblast-mediated resistance in hepatocellular carcinoma: emerging therapeutic vulnerabilities and targeting strategies.Cancer gene therapy · 2026Review
- Remodeling the Stroma: The Role of ncRNAs in Cancer-Associated Fibroblasts and Therapeutic Implications for Digestive Tumors.Drug design, development and therapy · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is an aggressive malignancy with poor prognosis. LncRNA MAPKAPK5-AS1 is a potential oncogene and contributes to HCC cell malignant proliferation. This study explores the role of MAPKAPK5-AS1 carried by carcinoma-associated fibroblasts-derived extracellular vesicles (CAF-EVs) in HCC cell proliferation. Our findings reveal that CAF-EVs promotes HCC cell proliferation by delivering MAPKAPK5-AS1, which binds to and inhibits SMURF2 and stabilizes TCF12. SMURF2 leads to TCF12 ubiquitination and degradation. TCF12 upregulates FOXH1 expression. In animal model, CAF-EVs enhances tumor growth by stabilizing TCF12 via MAPKAPK5-AS1 and activating FOXH1 transcription. In conclusion, CAF-EVs carrying MAPKAPK5-AS1 stabilizes TCF12 expression by competitively inhibiting SMURF2, thus promoting TCF12-mediated FOXH1 transcription and driving HCC cell proliferation. Our findings may offer insights for HCC treatment and suggest potential targets for future treatments, opening avenues for HCC therapies.
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Registered trials
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