Mitochondrial Ribosomal Protein Family in Cancers: Mechanistic Insights and Therapeutic Implications

ABSTRACT Mitochondria, as the main site for aerobic respiration in cells, are indispensable participants in the reprogrammed metabolic activities of tumor cells. Mitochondrial ribosomal proteins (MRPs), essential components of the mitochondrial ribosome (mitoribosome), play a critical role in mainta...

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Main Authors: Qian Chen, Yingli Zhang, Jin‐Jian Lu, Ting Li
Format: Article
Language:English
Published: Wiley 2025-06-01
Series:MedComm – Oncology
Subjects:
Online Access:https://doi.org/10.1002/mog2.70024
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author Qian Chen
Yingli Zhang
Jin‐Jian Lu
Ting Li
author_facet Qian Chen
Yingli Zhang
Jin‐Jian Lu
Ting Li
author_sort Qian Chen
collection DOAJ
description ABSTRACT Mitochondria, as the main site for aerobic respiration in cells, are indispensable participants in the reprogrammed metabolic activities of tumor cells. Mitochondrial ribosomal proteins (MRPs), essential components of the mitochondrial ribosome (mitoribosome), play a critical role in maintaining mitochondrial function and regulating oncogenic signaling. Their molecular mechanisms and biological functions make MRPs key regulators of tumorigenesis, drug resistance, and tumor immune escape. MRPs are abnormally expressed in various cancer types and are linked to the prognosis of cancer patients. However, a thorough grasp of the specific mechanisms and a holistic analysis of the relationship between MRPs and different cancers are lacking. This review highlights the specific regulatory roles of MRPs, including MRPS5, MRPS29, MRPL9, MRPL12, MRPL13, MRPL33, MRPL58, and MRPL59, in cancer. Additionally, we examine the potential of MRPs as prospective clinical biomarkers and discuss their relationship with clinical prognosis and treatment response. We further explore the underlying reasons for the diverse functions of MRPs, their implications in cellular signaling and tumor immunity, and consider the prospects for developing MRP inhibitors as therapeutic strategies. Our comprehensive analysis deepens the understanding of MRPs complex biological functions and emphasizes their promising potential as therapeutic targets in cancer treatment.
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spelling doaj-art-e0456817af5e4581ba336e13c1dd35492025-08-20T03:32:14ZengWileyMedComm – Oncology2769-64482025-06-0142n/an/a10.1002/mog2.70024Mitochondrial Ribosomal Protein Family in Cancers: Mechanistic Insights and Therapeutic ImplicationsQian Chen0Yingli Zhang1Jin‐Jian Lu2Ting Li3State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences University of Macau Macao ChinaZhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM) Chinese Academy of Sciences Hangzhou Zhejiang ChinaState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences University of Macau Macao ChinaState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences University of Macau Macao ChinaABSTRACT Mitochondria, as the main site for aerobic respiration in cells, are indispensable participants in the reprogrammed metabolic activities of tumor cells. Mitochondrial ribosomal proteins (MRPs), essential components of the mitochondrial ribosome (mitoribosome), play a critical role in maintaining mitochondrial function and regulating oncogenic signaling. Their molecular mechanisms and biological functions make MRPs key regulators of tumorigenesis, drug resistance, and tumor immune escape. MRPs are abnormally expressed in various cancer types and are linked to the prognosis of cancer patients. However, a thorough grasp of the specific mechanisms and a holistic analysis of the relationship between MRPs and different cancers are lacking. This review highlights the specific regulatory roles of MRPs, including MRPS5, MRPS29, MRPL9, MRPL12, MRPL13, MRPL33, MRPL58, and MRPL59, in cancer. Additionally, we examine the potential of MRPs as prospective clinical biomarkers and discuss their relationship with clinical prognosis and treatment response. We further explore the underlying reasons for the diverse functions of MRPs, their implications in cellular signaling and tumor immunity, and consider the prospects for developing MRP inhibitors as therapeutic strategies. Our comprehensive analysis deepens the understanding of MRPs complex biological functions and emphasizes their promising potential as therapeutic targets in cancer treatment.https://doi.org/10.1002/mog2.70024mitochondriamitochondrial ribosomal proteins familyoxidative phosphorylation (OXPHOS)tumorigenesis
spellingShingle Qian Chen
Yingli Zhang
Jin‐Jian Lu
Ting Li
Mitochondrial Ribosomal Protein Family in Cancers: Mechanistic Insights and Therapeutic Implications
MedComm – Oncology
mitochondria
mitochondrial ribosomal proteins family
oxidative phosphorylation (OXPHOS)
tumorigenesis
title Mitochondrial Ribosomal Protein Family in Cancers: Mechanistic Insights and Therapeutic Implications
title_full Mitochondrial Ribosomal Protein Family in Cancers: Mechanistic Insights and Therapeutic Implications
title_fullStr Mitochondrial Ribosomal Protein Family in Cancers: Mechanistic Insights and Therapeutic Implications
title_full_unstemmed Mitochondrial Ribosomal Protein Family in Cancers: Mechanistic Insights and Therapeutic Implications
title_short Mitochondrial Ribosomal Protein Family in Cancers: Mechanistic Insights and Therapeutic Implications
title_sort mitochondrial ribosomal protein family in cancers mechanistic insights and therapeutic implications
topic mitochondria
mitochondrial ribosomal proteins family
oxidative phosphorylation (OXPHOS)
tumorigenesis
url https://doi.org/10.1002/mog2.70024
work_keys_str_mv AT qianchen mitochondrialribosomalproteinfamilyincancersmechanisticinsightsandtherapeuticimplications
AT yinglizhang mitochondrialribosomalproteinfamilyincancersmechanisticinsightsandtherapeuticimplications
AT jinjianlu mitochondrialribosomalproteinfamilyincancersmechanisticinsightsandtherapeuticimplications
AT tingli mitochondrialribosomalproteinfamilyincancersmechanisticinsightsandtherapeuticimplications