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Peer-reviewedCC BY 4.0Cell Death Discovery

SNORD18B/SNORD18C-RPL23A promotes homologous recombination repair by regulating BRCA1 translation in colorectal cancer cells

  • Chuxian Lin1
  • Junyan He2
  • Lei Wu1
  • Xin Liu1
  • Ying Fan1
  • Dan Cai3
  • Meng Jia1
  • Wencheng Zhang1
  • Qi Wang1
  • Yaqiong Li1
  • Ruixue Liu1
  • Wenqing Lu1
6 more authors
  • Jianan Ma1
  • MaoXiang Zhu1
  • Pingkun Zhou1
  • Zhenhua Qi1
  • Liping Shen1
  • Zhidong Wang1,3
  1. 1Beijing Institute of Radiation Medicine, Beijing, China
  2. 2Department of Oncology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, China
  3. 3Graduate Collaborative Training Base of Academy of Military Sciences, Hengyang Medical School, University of South China, Hengyang, China
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Abstract

Homologous recombination (HR) is one of the classical pathways for repairing DNA double-strand breaks (DSBs), a type of lesion that poses a severe threat to genomic stability and cell survival. The role of small nucleolar RNAs (snoRNAs), particularly their interactions with ribosomal proteins, in the HR repair has not been reported. This is the first study to report the role of snoRNA genes SNORD18B and SNORD18C (SNORD18B/C) in HR repair, demonstrating that they exert an oncogenic function in colorectal cancer (CRC) by promoting cell proliferation and radioresistance. Mechanistically, SNORD18B/C directly interacts with the ribosomal protein RPL23A to enhance the translation of BRCA1 independent of the canonical 2′-O-methylation of 28S rRNA, thereby promoting HR efficiency to facilitate radiation-induced DSB repair. Collectively, our findings confirm that the SNORD18B/C-RPL23A-BRCA1 axis is crucial for HR repair and highlight the SNORD18B/C as potential CRC therapeutic targets.

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Cite

BibTeXRIS
BibTeX
@article{lin2026snord18bsnord18crpl23a,
  title = {{SNORD18B/SNORD18C-RPL23A promotes homologous recombination repair by regulating BRCA1 translation in colorectal cancer cells}},
  author = {Chuxian Lin and Junyan He and Lei Wu and Xin Liu and Ying Fan and Dan Cai and Meng Jia and Wencheng Zhang and Qi Wang and Yaqiong Li and Ruixue Liu and Wenqing Lu and Jianan Ma and MaoXiang Zhu and Pingkun Zhou and Zhenhua Qi and Liping Shen and Zhidong Wang},
  journal = {Cell Death Discovery},
  year = {2026},
  month = aug,
  doi = {10.1038/s41420-026-03289-3},
  url = {https://doi.org/10.1038/s41420-026-03289-3},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - SNORD18B/SNORD18C-RPL23A promotes homologous recombination repair by regulating BRCA1 translation in colorectal cancer cells
AU  - Chuxian Lin
AU  - Junyan He
AU  - Lei Wu
AU  - Xin Liu
AU  - Ying Fan
AU  - Dan Cai
AU  - Meng Jia
AU  - Wencheng Zhang
AU  - Qi Wang
AU  - Yaqiong Li
AU  - Ruixue Liu
AU  - Wenqing Lu
AU  - Jianan Ma
AU  - MaoXiang Zhu
AU  - Pingkun Zhou
AU  - Zhenhua Qi
AU  - Liping Shen
AU  - Zhidong Wang
PY  - 2026
DA  - 2026/08/06
JO  - Cell Death Discovery
DO  - 10.1038/s41420-026-03289-3
UR  - https://doi.org/10.1038/s41420-026-03289-3
AB  - Homologous recombination (HR) is one of the classical pathways for repairing DNA double-strand breaks (DSBs), a type of lesion that poses a severe threat to genomic stability and cell survival. The role of small nucleolar RNAs (snoRNAs), particularly their interactions with ribosomal proteins, in the HR repair has not been reported. This is the first study to report the role of snoRNA genes SNORD18B and SNORD18C (SNORD18B/C) in HR repair, demonstrating that they exert an oncogenic function in colorectal cancer (CRC) by promoting cell proliferation and radioresistance. Mechanistically, SNORD18B/C directly interacts with the ribosomal protein RPL23A to enhance the translation of BRCA1 independent of the canonical 2′-O-methylation of 28S rRNA, thereby promoting HR efficiency to facilitate radiation-induced DSB repair. Collectively, our findings confirm that the SNORD18B/C-RPL23A-BRCA1 axis is crucial for HR repair and highlight the SNORD18B/C as potential CRC therapeutic targets.
SN  - 2058-7716
ER  -