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Peer-reviewedCC BY-NC-NDBiology direct

Targeting MRPL37 disrupts the pro-tumorigenic mitochondrial cascade in bladder cancer: from LRPPRC deficiency to ROS/AKT axis inhibition.

  • Xieyuan Leng1,2
  • Wenhao Lu3
  • Rongbin Zhou1,2
  • Chengbang Wang1,2
  • Zuheng Wang1,2
  • Haodong Peng1,2
  • Yitong Guo1,2
  • Baoyu Huang1,2
  • Dongwei Pan4
  • Dianyu Wang1,2
  • Zequn Su1,2
  • Xuanfan Liu5
8 more authors
  • Xuefang Liang1
  • Tian Guo1
  • Wen Liang1
  • Wentin Chen1
  • Zihang Huang1
  • Zhe Chen6
  • Yigan Zhang7,8
  • Fubo Wang9,10
10 affiliations
  1. 1Center for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, University Engineering Research Center of Digital Medicine and Healthcare, Guangxi Medical University, Nanning, Guangxi, 530021, China.
  2. 2School of Life Sciences, Guangxi Medical University, Nanning, Guangxi, China.
  3. 3Department of Urology, Guangxi Hospital Division of the First Affiliated Hospital, Sun Yat-sen University, Nanning, Guangxi, 530022, China.
  4. 4Department of Urology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, China.
  5. 5Department of Urology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, P.R. China.
  6. 6Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  7. 7Institute of Biomedical Research, Department of Infectious Diseases, Regulatory Mechanism and Targeted Therapy for Liver Cancer Shiyan Key Laboratory, Hubei Provincial Clinical Research Center for Precise Diagnosis and Treatment of Liver Cancer, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, 442000, China. [email protected].
  8. 8Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, 442000, China. [email protected].
  9. 9Center for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, University Engineering Research Center of Digital Medicine and Healthcare, Guangxi Medical University, Nanning, Guangxi, 530021, China. [email protected].
  10. 10School of Life Sciences, Guangxi Medical University, Nanning, Guangxi, China. [email protected].
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Abstract

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.

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Cite

BibTeXRIS
BibTeX
@article{leng2026targeting,
  title = {{Targeting MRPL37 disrupts the pro-tumorigenic mitochondrial cascade in bladder cancer: from LRPPRC deficiency to ROS/AKT axis inhibition.}},
  author = {Xieyuan Leng and Wenhao Lu and Rongbin Zhou and Chengbang Wang and Zuheng Wang and Haodong Peng and Yitong Guo and Baoyu Huang and Dongwei Pan and Dianyu Wang and Zequn Su and Xuanfan Liu and Xuefang Liang and Tian Guo and Wen Liang and Wentin Chen and Zihang Huang and Zhe Chen and Yigan Zhang and Fubo Wang},
  journal = {Biology direct},
  year = {2026},
  month = jul,
  doi = {10.1186/s13062-026-00883-4},
  url = {https://europepmc.org/article/MED/42928237},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Targeting MRPL37 disrupts the pro-tumorigenic mitochondrial cascade in bladder cancer: from LRPPRC deficiency to ROS/AKT axis inhibition.
AU  - Xieyuan Leng
AU  - Wenhao Lu
AU  - Rongbin Zhou
AU  - Chengbang Wang
AU  - Zuheng Wang
AU  - Haodong Peng
AU  - Yitong Guo
AU  - Baoyu Huang
AU  - Dongwei Pan
AU  - Dianyu Wang
AU  - Zequn Su
AU  - Xuanfan Liu
AU  - Xuefang Liang
AU  - Tian Guo
AU  - Wen Liang
AU  - Wentin Chen
AU  - Zihang Huang
AU  - Zhe Chen
AU  - Yigan Zhang
AU  - Fubo Wang
PY  - 2026
DA  - 2026/07/29
JO  - Biology direct
DO  - 10.1186/s13062-026-00883-4
UR  - https://europepmc.org/article/MED/42928237
AB  - 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.
SN  - 1745-6150
ER  -