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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Antitumor effect of arsenic trioxide in murine xenograft model
Mariko Kito1, Kenji Matsumoto, Naoko Wada
1Institute of Applied Biochemistry, Yagi Memorial Park, Mitake, Kani-gun, Gifu 505-0116.
Abstract:
Arsenic trioxide, As(2)O(3) (ATO), has been established to be an effective agent for treating acute promyelocytic leukemia, but its effect on solid tumors has not been fully explored. In the present study in a murine xenograft system, we found that ATO significantly inhibited tumor growth of the inoculated human hepatocellular carcinoma cell line HuH7 when administered either intravenously or intratumorally. Pathological examination revealed that ATO induced extensive cell death in the tumor. Some of the dead cells in intratumorally ATO-treated mice showed characteristic features of apoptosis, such as nuclear condensation and fragmentation, and were TUNEL-positive. The measurement of arsenic by using particle induced X-ray emission revealed that arsenic was accumulated more in the tumor than in brain, kidney or liver after the intravenous injection of ATO, which is consistent with the hemorrhagic cell death observed in ATO-treated tumor tissues. Thus, ATO appears to have potential for the treatment of solid tumors, as well as hematopoietic malignancies.
Insights
Arsenic trioxide (ATO) effectively targets hepatocellular carcinoma in mice, inhibiting tumor growth and causing cell death. This suggests ATO
Area of Science:
- Oncology
- Pharmacology
- Biochemistry
Background:
- Arsenic trioxide (ATO) is a validated treatment for acute promyelocytic leukemia.
- The efficacy of ATO against solid tumors remains largely uninvestigated.
Purpose of the Study:
- To evaluate the anti-tumorigenic effects of arsenic trioxide (ATO) on human hepatocellular carcinoma (HuH7) in a murine xenograft model.
- To investigate the mechanisms of tumor cell death induced by ATO.
Main Methods:
- Murine xenograft model inoculated with human hepatocellular carcinoma (HuH7) cells.
- Administration of arsenic trioxide (ATO) via intravenous and intratumoral routes.
- Pathological examination, including apoptosis assessment (TUNEL assay) and arsenic quantification (particle-induced X-ray emission).
Main Results:
- Arsenic trioxide (ATO) significantly inhibited hepatocellular carcinoma tumor growth in vivo.
- ATO induced extensive tumor cell death, with features of apoptosis observed.
- Arsenic accumulation was higher in tumor tissues compared to other organs after intravenous administration.
Conclusions:
- Arsenic trioxide (ATO) demonstrates significant potential for treating solid tumors, including hepatocellular carcinoma.
- ATO-induced tumor cell death and accumulation in tumor tissues support its therapeutic application.
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