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Peer-reviewedCC BYCell death & disease

Targeting RBM41-mediated CKMT1B mRNA stability triggers disulfidptosis and suppresses tongue squamous cell carcinoma.

  • Boqiang Tao1,2
  • Ming Hao1,2
  • Yang Hao3
  • Shuhan Zhang3
  • Zhaorong Xiao1,2
  • He Shi1,2
  • Qirong Li3
  • Yiwen Qin1,2
  • Dongxu Wang4
  • Weiwei Liu5,6
6 affiliations
  1. 1Department of Oral and Maxillofacial Surgery, Hospital of Stomatology, Jilin University, Changchun, China.
  2. 2Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Hospital of Stomatology, Jilin University, Changchun, China.
  3. 3Laboratory Animal Center, College of Animal Science, Jilin University, Changchun, China.
  4. 4Laboratory Animal Center, College of Animal Science, Jilin University, Changchun, China. [email protected].
  5. 5Department of Oral and Maxillofacial Surgery, Hospital of Stomatology, Jilin University, Changchun, China. [email protected].
  6. 6Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Hospital of Stomatology, Jilin University, Changchun, China. [email protected].
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Abstract

Clarifying the mechanisms by which metabolic stress induces cell death in tumor cells is essential for the development of effective therapies targeting tongue squamous cell carcinoma (TSCC). In this study, we demonstrate that the RNA-binding motif protein 41 (RBM41) stabilizes CKMT1B mRNA through its RRM1 domain, thereby conferring resistance to disulfidptosis under conditions of glucose deprivation in TSCC. We explored the expression and functional role of RBM41 using both in vitro and in vivo models, which included RBM41-knockout, RRM1-domain-knockout, and RBM41-overexpressing TSCC cell lines. Our findings reveal that RBM41-mediated stabilization of CKMT1B mRNA is crucial for protecting TSCC cells from disulfidptosis during metabolic stress. Based on this mechanism, we designed a structure-specific inhibitory small molecule, L759-0762, which disrupts the interaction between RBM41 and CKMT1B mRNA. L759-0762 selectively sensitizes TSCC cells to disulfidptosis under glucose deprivation by abolishing the protective function of RBM41. Collectively, our findings identify RBM41 as a viable therapeutic target and demonstrate that pharmacological disruption of its interaction with CKMT1B mRNA represents a promising strategy for inducing disulfidptosis in TSCC.

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Cite

BibTeXRIS
BibTeX
@article{tao2026targeting,
  title = {{Targeting RBM41-mediated CKMT1B mRNA stability triggers disulfidptosis and suppresses tongue squamous cell carcinoma.}},
  author = {Boqiang Tao and Ming Hao and Yang Hao and Shuhan Zhang and Zhaorong Xiao and He Shi and Qirong Li and Yiwen Qin and Dongxu Wang and Weiwei Liu},
  journal = {Cell death \& disease},
  year = {2026},
  month = jul,
  doi = {10.1038/s41419-026-09166-2},
  url = {https://europepmc.org/article/MED/42957673},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Targeting RBM41-mediated CKMT1B mRNA stability triggers disulfidptosis and suppresses tongue squamous cell carcinoma.
AU  - Boqiang Tao
AU  - Ming Hao
AU  - Yang Hao
AU  - Shuhan Zhang
AU  - Zhaorong Xiao
AU  - He Shi
AU  - Qirong Li
AU  - Yiwen Qin
AU  - Dongxu Wang
AU  - Weiwei Liu
PY  - 2026
DA  - 2026/07/31
JO  - Cell death & disease
DO  - 10.1038/s41419-026-09166-2
UR  - https://europepmc.org/article/MED/42957673
AB  - Clarifying the mechanisms by which metabolic stress induces cell death in tumor cells is essential for the development of effective therapies targeting tongue squamous cell carcinoma (TSCC). In this study, we demonstrate that the RNA-binding motif protein 41 (RBM41) stabilizes CKMT1B mRNA through its RRM1 domain, thereby conferring resistance to disulfidptosis under conditions of glucose deprivation in TSCC. We explored the expression and functional role of RBM41 using both in vitro and in vivo models, which included RBM41-knockout, RRM1-domain-knockout, and RBM41-overexpressing TSCC cell lines. Our findings reveal that RBM41-mediated stabilization of CKMT1B mRNA is crucial for protecting TSCC cells from disulfidptosis during metabolic stress. Based on this mechanism, we designed a structure-specific inhibitory small molecule, L759-0762, which disrupts the interaction between RBM41 and CKMT1B mRNA. L759-0762 selectively sensitizes TSCC cells to disulfidptosis under glucose deprivation by abolishing the protective function of RBM41. Collectively, our findings identify RBM41 as a viable therapeutic target and demonstrate that pharmacological disruption of its interaction with CKMT1B mRNA represents a promising strategy for inducing disulfidptosis in TSCC.
SN  - 2041-4889
ER  -