UBASH3B-mediated MRPL12 Y60 dephosphorylation inhibits LUAD development by driving mitochondrial metabolism reprogramming
This study establishes MRPL12 as a novel oncogene in LUAD, contributing to LUAD pathogenesis by orchestrating mitochondrial metabolism reprogramming towards oxidative phosphorylation (OXPHOS). Furthermore, it confirms Y60 as a specific phosphorylation modification site regulating MRPL12's oncogenic functions, offering insights for the development of LUAD-specific targeted drugs and clinical interventions.
Authors
- Qiang Wan (ORCID: https://orcid.org/0000-0001-9173-2941)
- Weiying Zhang (ORCID: https://orcid.org/0000-0001-5880-1933)
- Li Xu (ORCID: https://orcid.org/0000-0003-4405-1048)
- Jian Sun (ORCID: https://orcid.org/0000-0002-4868-5905)
- Tianyi Zhang (ORCID: https://orcid.org/0000-0002-2833-3363)
- Xueru Cao
- Xiaojia Song
- Shengnan Sun (ORCID: https://orcid.org/0009-0005-3842-8090)
- Fuyuan Xue
- Yi Liu (ORCID: https://orcid.org/0000-0002-2207-8074)
- Yongjian Jing
- Xingzhao Ji
- Guoyuan Ma
Institutions
- Shandong Provincial Hospital (CN)
- Boxing People's Hospital (CN)
- Heze Municipal Hospital (CN)
- Shandong First Medical University (CN)
Publication Details
- Journal
- Journal of Experimental & Clinical Cancer Research
- Published
- 2024-09-30
- DOI
- https://doi.org/10.1186/s13046-024-03181-x
- Citations
- 9
- Primary Topic
- Cancer, Hypoxia, and Metabolism
- Type
- article
- Field-Weighted Citation Impact
- 2.57
Funders
- National Natural Science Foundation of China
- Natural Science Foundation of Shandong Province
- Shandong First Medical University