ArticleiScience2025
MRPL37 promotes hepatocellular carcinoma progression through modulating mitochondrial energy metabolism.
Article in iScience, 2025. 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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Dual regulation of metabolic reprogramming and protein competitive modifications: the core role and mechanism of MRPL36 in glioblastoma malignant progression.Journal of experimental & clinical cancer research : CR · 2026Article
- Mitochondrial ribosomal protein MRPL27 supports glioma malignancy through regulation of oxidative phosphorylation.Cellular and molecular life sciences : CMLS · 2026Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial ribosomal proteins of the large subunit (MRPLs) are critical for mitochondrial function and cellular energy metabolism. However, the role of the MRPL family in hepatocellular carcinoma (HCC) remains poorly understood. Here, we leveraged The Cancer Genome Atlas (TCGA) liver cancer data to develop a subtype classification and prognostic model based on the MRPL family genes, identifying MRPL37 as a key gene associated with HCC progression. Clinically, MRPL37 upregulation is associated with HCC progression and poor prognosis. Functionally, MRPL37 knockdown significantly inhibits HCC cell proliferation, disrupts cell cycle progression, and induces apoptosis
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Registered trials
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