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Peer-reviewedCC BY-NC-ND 4.0International Journal of Molecular Medicine

From RNA fate to cancer state transitions: m5C-driven metabolic and immune reprogramming (Review)

  • Yuanli Zhou1,2
  • Bolv Zhu1,2
  • Xingzhou Tang1,3
  • Shuishui Yin1,4
4 affiliations
  1. 1Second Clinical Medical College, Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou 550001, P.R. China
  2. 2Department of Gynecology, The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou 550001, P.R. China
  3. 3Department of Proctology, The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou 550001, P.R. China
  4. 4Department of Oncology, The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou 550001, P.R. China
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Abstract

RNA 5-methylcytosine (m5C) regulates RNA stability, processing and translation, linking changes in nutrient supply and stress to cancer-cell behavior. Its consequences depend on the RNA substrate and the proteins that recognize or process the modification. This dependence helps explain why NOP2/Sun RNA methyltransferase 2 (NSUN2), NOP2 nucleolar protein, NSUN5, NSUN6 and tRNA aspartic acid methyltransferase 1 can affect proliferation, metabolism, immunity and treatment response differently. Across coding and noncoding RNAs, m5C regulation can sustain growth-related protein expression, alter DNA damage repair and support metabolic defenses against cell death. Metabolites also regulate writers and readers, creating feedback in specific tumor models that connects nutrient availability with RNA recognition. These relationships suggest several therapeutic approaches, including nucleoside analogues, writer or reader inhibition, substrate-RNA targeting and tumor-directed delivery. Experimental combinations can restore drug sensitivity, although simultaneous effects on immune cells or normal tissues may limit systemic treatment. Clinical translation requires relating treatment-induced RNA changes to drug exposure, tumor selectivity and immune-cell function, rather than relying on regulator expression alone.

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Cite

BibTeXRIS
BibTeX
@article{zhou2026from,
  title = {{From RNA fate to cancer state transitions: m5C-driven metabolic and immune reprogramming (Review)}},
  author = {Yuanli Zhou and Bolv Zhu and Xingzhou Tang and Shuishui Yin},
  journal = {International Journal of Molecular Medicine},
  year = {2026},
  month = oct,
  doi = {10.3892/ijmm.2026.6019},
  url = {https://doi.org/10.3892/ijmm.2026.6019},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - From RNA fate to cancer state transitions: m5C-driven metabolic and immune reprogramming (Review)
AU  - Yuanli Zhou
AU  - Bolv Zhu
AU  - Xingzhou Tang
AU  - Shuishui Yin
PY  - 2026
DA  - 2026/10/20
JO  - International Journal of Molecular Medicine
DO  - 10.3892/ijmm.2026.6019
UR  - https://doi.org/10.3892/ijmm.2026.6019
AB  - RNA 5-methylcytosine (m5C) regulates RNA stability, processing and translation, linking changes in nutrient supply and stress to cancer-cell behavior. Its consequences depend on the RNA substrate and the proteins that recognize or process the modification. This dependence helps explain why NOP2/Sun RNA methyltransferase 2 (NSUN2), NOP2 nucleolar protein, NSUN5, NSUN6 and tRNA aspartic acid methyltransferase 1 can affect proliferation, metabolism, immunity and treatment response differently. Across coding and noncoding RNAs, m5C regulation can sustain growth-related protein expression, alter DNA damage repair and support metabolic defenses against cell death. Metabolites also regulate writers and readers, creating feedback in specific tumor models that connects nutrient availability with RNA recognition. These relationships suggest several therapeutic approaches, including nucleoside analogues, writer or reader inhibition, substrate-RNA targeting and tumor-directed delivery. Experimental combinations can restore drug sensitivity, although simultaneous effects on immune cells or normal tissues may limit systemic treatment. Clinical translation requires relating treatment-induced RNA changes to drug exposure, tumor selectivity and immune-cell function, rather than relying on regulator expression alone.
SN  - 1107-3756
SN  - 1791-244X
ER  -