Vaccination Efficacy of Mitoxantrone-Treated CT-26 Cells Under Different Drug Concentrations and Vaccination Intervals
4 affiliations
- 1KM Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon 34054, Republic of Korea
- 2Department of Pharmaceutical Engineering, Gyeongsang National University, Jinju 52828, Republic of Korea
- 3Department of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea
- 4KIOM School, University of Science & Technology (UST), Daejeon 34054, Republic of Korea
Abstract
Immunogenic cell death (ICD) converts dying tumor cells into an anticancer vaccine, yet whether protection depends on how those cells are prepared and when they are given has rarely been examined. Using mitoxantrone (MTX), a clinically approved small molecule classified as an ICD inducer, we examined both variables in the murine CT-26 colon carcinoma model. MTX reduced viability in a concentration-dependent manner and induced extracellular ATP release. The total extent of cell death, however, was similar across concentrations, indicating that the concentration-dependent loss of viability was not accompanied by a proportional increase in cell death. What differed was the composition of the dying population, which shifted from early to late apoptotic cells as the concentration increased. Prophylactic vaccination with MTX-treated cells protected BALB/c mice, leaving 75.0–87.5% of animals tumor-free after vaccination at 1 μM and 37.5–62.5% at 3 μM across independent experiments. Protection increased with the interval between vaccination and challenge, with 0%, 50.0%, and 87.5% of animals tumor-free after simultaneous injection, a 3-day interval, and a 7-day interval, respectively. Cells killed completely by freeze–thaw were inactive as a vaccine, and cisplatin-treated cells conferred only a marginal delay, whereas responders to MTX-treated cells resisted rechallenge for the remainder of the observation period. Taken together, these results show that use of an ICD-inducing drug alone is not sufficient for effective dying-cell vaccination and that protective efficacy is influenced by vaccine preparation and by the interval between vaccination and tumor challenge, rather than by the extent of cell death alone.
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BibTeX
@article{na2026vaccination,
title = {{Vaccination Efficacy of Mitoxantrone-Treated CT-26 Cells Under Different Drug Concentrations and Vaccination Intervals}},
author = {Se Won Na and Mibae Jeong and Mi-Kyung Jeong and Jaemoo Chun},
journal = {Molecules},
year = {2026},
month = oct,
doi = {10.3390/molecules31213827},
url = {https://www.mdpi.com/1420-3049/31/21/3827},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Vaccination Efficacy of Mitoxantrone-Treated CT-26 Cells Under Different Drug Concentrations and Vaccination Intervals
AU - Se Won Na
AU - Mibae Jeong
AU - Mi-Kyung Jeong
AU - Jaemoo Chun
PY - 2026
DA - 2026/10/23
JO - Molecules
DO - 10.3390/molecules31213827
UR - https://www.mdpi.com/1420-3049/31/21/3827
AB - Immunogenic cell death (ICD) converts dying tumor cells into an anticancer vaccine, yet whether protection depends on how those cells are prepared and when they are given has rarely been examined. Using mitoxantrone (MTX), a clinically approved small molecule classified as an ICD inducer, we examined both variables in the murine CT-26 colon carcinoma model. MTX reduced viability in a concentration-dependent manner and induced extracellular ATP release. The total extent of cell death, however, was similar across concentrations, indicating that the concentration-dependent loss of viability was not accompanied by a proportional increase in cell death. What differed was the composition of the dying population, which shifted from early to late apoptotic cells as the concentration increased. Prophylactic vaccination with MTX-treated cells protected BALB/c mice, leaving 75.0–87.5% of animals tumor-free after vaccination at 1 μM and 37.5–62.5% at 3 μM across independent experiments. Protection increased with the interval between vaccination and challenge, with 0%, 50.0%, and 87.5% of animals tumor-free after simultaneous injection, a 3-day interval, and a 7-day interval, respectively. Cells killed completely by freeze–thaw were inactive as a vaccine, and cisplatin-treated cells conferred only a marginal delay, whereas responders to MTX-treated cells resisted rechallenge for the remainder of the observation period. Taken together, these results show that use of an ICD-inducing drug alone is not sufficient for effective dying-cell vaccination and that protective efficacy is influenced by vaccine preparation and by the interval between vaccination and tumor challenge, rather than by the extent of cell death alone.
SN - 1420-3049
ER -