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Peer-reviewedCC BYFrontiers in molecular neuroscience

miR-378f targets CAB39 to regulate autophagy in chemotherapy-induced peripheral neuropathy.

  • Yeeun Kim1,2
  • Myeongguk Jeong2,3
  • Hyeokjin Kwon2
  • Jungho Kim2,4
  • Yeongdon Ju5
  • Do-Young Kang1,6
  • Aelee Jang7
  • Go-Eun Choi2,4
7 affiliations
  1. 1Department of Translational Biomedical Sciences, Graduate School of Dong-A University, Busan, Republic of Korea.
  2. 2Department of Clinical Laboratory Science, College of Health Sciences, Catholic University of Pusan, Busan, Republic of Korea.
  3. 3Research Center for Endocrine and Metabolic Diseases, Convergence Medical Institute, Chungnam National University, Daejeon, Republic of Korea.
  4. 4Next-Generation Industrial Field-Based Specialist Program for Molecular Diagnostics, Brain Busan 21 Plus Project, Graduate School, Catholic University of Pusan, Busan, Republic of Korea.
  5. 5Department of Biomedical Laboratory Science, Gimcheon University, Gimcheon, Republic of Korea.
  6. 6Department of Nuclear Medicine, Dong-A University College of Medicine, Busan, Republic of Korea.
  7. 7Department of Nursing, University of Ulsan, Ulsan, Republic of Korea.
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Abstract

Chemotherapy is the most common cancer therapy due to its ability to effectively destroy cancer cells. However, peripheral neuropathy is a notable side effect, which has no clearly established prevention or treatment methods. Although various therapeutic strategies using microRNAs (miRNAs) have been developed for a wide range of diseases, the role of miRNAs in neuroregeneration has yet to be elucidated. Our group previously identified five differentially expressed miRNAs in the plasma of patients with gastric cancer receiving XELOX (capecitabine and oxaliplatin) chemotherapy. Among these, miR-378f alone showed a significant correlation with peripheral neuropathy severity, providing the rationale for the present study. Bioinformatic analysis further predicted calcium-binding protein 39 (CAB39), a regulator of autophagy, as a shared target of these miRNAs. The downregulation of miR-378f increased CAB39 expression, activated AMPK and inhibited mTOR. Furthermore, changes in autophagy-related markers were observed, including increased Beclin-1 expression, elevated LC3-I to LC3-II conversion, and decreased p62 expression. The findings of the present study suggest that autophagy regulation by miR-378f may be a novel diagnostic and therapeutic target for peripheral neuropathy.

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Cite

BibTeXRIS
BibTeX
@article{kim2026mir378f,
  title = {{miR-378f targets CAB39 to regulate autophagy in chemotherapy-induced peripheral neuropathy.}},
  author = {Yeeun Kim and Myeongguk Jeong and Hyeokjin Kwon and Jungho Kim and Yeongdon Ju and Do-Young Kang and Aelee Jang and Go-Eun Choi},
  journal = {Frontiers in molecular neuroscience},
  year = {2026},
  month = oct,
  doi = {10.3389/fnmol.2026.1958322},
  url = {https://europepmc.org/article/MED/42908948},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - miR-378f targets CAB39 to regulate autophagy in chemotherapy-induced peripheral neuropathy.
AU  - Yeeun Kim
AU  - Myeongguk Jeong
AU  - Hyeokjin Kwon
AU  - Jungho Kim
AU  - Yeongdon Ju
AU  - Do-Young Kang
AU  - Aelee Jang
AU  - Go-Eun Choi
PY  - 2026
DA  - 2026/10/07
JO  - Frontiers in molecular neuroscience
DO  - 10.3389/fnmol.2026.1958322
UR  - https://europepmc.org/article/MED/42908948
AB  - Chemotherapy is the most common cancer therapy due to its ability to effectively destroy cancer cells. However, peripheral neuropathy is a notable side effect, which has no clearly established prevention or treatment methods. Although various therapeutic strategies using microRNAs (miRNAs) have been developed for a wide range of diseases, the role of miRNAs in neuroregeneration has yet to be elucidated. Our group previously identified five differentially expressed miRNAs in the plasma of patients with gastric cancer receiving XELOX (capecitabine and oxaliplatin) chemotherapy. Among these, miR-378f alone showed a significant correlation with peripheral neuropathy severity, providing the rationale for the present study. Bioinformatic analysis further predicted calcium-binding protein 39 (CAB39), a regulator of autophagy, as a shared target of these miRNAs. The downregulation of miR-378f increased CAB39 expression, activated AMPK and inhibited mTOR. Furthermore, changes in autophagy-related markers were observed, including increased Beclin-1 expression, elevated LC3-I to LC3-II conversion, and decreased p62 expression. The findings of the present study suggest that autophagy regulation by miR-378f may be a novel diagnostic and therapeutic target for peripheral neuropathy.
SN  - 1662-5099
ER  -