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Peer-reviewedCC BY 4.0Advanced Science

Amcinonide Exhibits Antitumor Effects in Radioresistant Colorectal Cancer Through the circRNF10/miR‐296‐5p/Snail Axis

  • Hyun Jeong Seok1
  • Dong Hyeon Lee1
  • Junhye Kwon2
  • Ui Sup Shin3
  • In Hwa Bae1
  1. 1Division of Radiation Biomedical Research Korea Institute of Radiological & Medical Sciences Seoul Republic of Korea
  2. 2Medical Sciences Substantiation Center Korea Cancer Center Hospital Korea Institute of Radiological & Medical Sciences Seoul Republic of Korea
  3. 3Department of Surgery Korea Cancer Center Hospital Korea Institute of Radiological & Medical Sciences Seoul Republic of Korea
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Abstract

Radiotherapy, commonly used in the treatment of colorectal cancer (CRC), can induce local recurrence and malignant progression in cases of intrinsic and acquired radioresistance; therefore, effective treatment strategies are required. In this study, we screened an FDA‐approved drug library and identified amcinonide (AMC), a topical corticosteroid, as a potential agent that inhibits radiation‐induced epithelial‐mesenchymal transition (EMT), cell migratory ability, and invasiveness in radioresistant colorectal cancer cells. Mechanistically, ionizing radiation‐induced circRNF10 suppressed miR‐296‐5p, thereby increasing Snail expression and promoting EMT and aggressive phenotypes in radioresistant CRC cells. We verified in vitro, in vivo, and in CRC patient‐derived organoids (PDOs) models that AMC suppresses the malignant phenotype by restoring miR‐296‐5p expression and reducing Snail expression. These findings identify the circRNF10/miR‐296‐5p/Snail axis as a key factor in CRC radioresistance and suggest that it may serve as a therapeutic target. Together, these results suggest that AMC is a promising drug for overcoming CRC radioresistance and that components of this axis may serve as potential diagnostic biomarkers. Overall, these findings highlight the therapeutic potential of targeting the ncRNA‐mediated EMT circuit to overcome radioresistant CRC.

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Cite

BibTeXRIS
BibTeX
@article{seok2026amcinonide,
  title = {{Amcinonide Exhibits Antitumor Effects in Radioresistant Colorectal Cancer Through the circRNF10/miR‐296‐5p/Snail Axis}},
  author = {Hyun Jeong Seok and Dong Hyeon Lee and Junhye Kwon and Ui Sup Shin and In Hwa Bae},
  journal = {Advanced Science},
  year = {2026},
  month = oct,
  doi = {10.1002/advs.78502},
  url = {https://doi.org/10.1002/advs.78502},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Amcinonide Exhibits Antitumor Effects in Radioresistant Colorectal Cancer Through the circRNF10/miR‐296‐5p/Snail Axis
AU  - Hyun Jeong Seok
AU  - Dong Hyeon Lee
AU  - Junhye Kwon
AU  - Ui Sup Shin
AU  - In Hwa Bae
PY  - 2026
DA  - 2026/10/26
JO  - Advanced Science
DO  - 10.1002/advs.78502
UR  - https://doi.org/10.1002/advs.78502
AB  - Radiotherapy, commonly used in the treatment of colorectal cancer (CRC), can induce local recurrence and malignant progression in cases of intrinsic and acquired radioresistance; therefore, effective treatment strategies are required. In this study, we screened an FDA‐approved drug library and identified amcinonide (AMC), a topical corticosteroid, as a potential agent that inhibits radiation‐induced epithelial‐mesenchymal transition (EMT), cell migratory ability, and invasiveness in radioresistant colorectal cancer cells. Mechanistically, ionizing radiation‐induced circRNF10 suppressed miR‐296‐5p, thereby increasing Snail expression and promoting EMT and aggressive phenotypes in radioresistant CRC cells. We verified in vitro, in vivo, and in CRC patient‐derived organoids (PDOs) models that AMC suppresses the malignant phenotype by restoring miR‐296‐5p expression and reducing Snail expression. These findings identify the circRNF10/miR‐296‐5p/Snail axis as a key factor in CRC radioresistance and suggest that it may serve as a therapeutic target. Together, these results suggest that AMC is a promising drug for overcoming CRC radioresistance and that components of this axis may serve as potential diagnostic biomarkers. Overall, these findings highlight the therapeutic potential of targeting the ncRNA‐mediated EMT circuit to overcome radioresistant CRC.
SN  - 2198-3844
ER  -