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Targeting MRPL37 disrupts the pro-tumorigenic mitochondrial cascade in bladder cancer: from LRPPRC deficiency to ROS/AKT axis inhibition
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DOI：10.1186/s13062-026-00883-4.png)
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Abstract
En 中文
Bladder cancer (BLCA) is a urinary system malignant tumor with high morbidity and mortality worldwide. There is an urgent need for new biomarkers and therapeutic targets. By integrating single-cell RNA sequencing, MitoCarta database and the Cancer Genome Atlas data, this study found that mitochondrial ribosomal protein L37 (MRPL37) was significantly up-regulated in BLCA, and its expression level was related to disease progression and poor prognosis. Functional experiments in vitro and in vivo confirmed that knockdown of MRPL37 could inhibit the proliferation, invasion, migration, metabolism and cisplatin resistance of BLCA cells by cell experiments, mouse subcutaneous tumor model, mouse orthotopic bladder cancer model and patient-derived organoid (PDO) model. A novel MRPL37-LRPPRC-ROS-AKT signaling axis was identified: loss of MRPL37 leads to the disorder of branched-chain amino acid metabolism, down-regulates the key mitochondrial protein LRPPRC, and then causes mitochondrial membrane potential damage and reactive oxygen species accumulation, which ultimately exert anti-cancer effect by inhibiting the AKT pathway. This study not only advances the understanding of the mechanism by which mitochondrial translation defects drive tumorigenesis, but also highlights the potential of MRPL37 as a target in BLCA prognosis and targeted therapy.
Keywords:
Bladder cancer
Mitochondrial tumor markers
MRPL37
Mitochondrial function
LRPPRC
ROS
AKT pathway
Organoids
Drug resistance
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