Journal
EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 22, Issue 1, Pages -Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2021.10173
Keywords
hirsutanol A; apoptosis; T-acute lymphocytic leukemia; p53
Categories
Funding
- Science and Technology Project of Health Commission of Sichuan [19PJ288]
- Key R&D projects of Sichuan Science and Technology Technology [2019YFS0531]
- Science and Technology Development Fund, Macau SAR [0013/2019/A1]
- [2019YJ0690]
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Hirsutanol A exhibits potential anticancer activity against T-acute lymphocytic leukemia Jurkat cells by inducing cell cycle arrest and p53-dependent apoptosis to inhibit cell viability.
Acute lymphocytic leukemia (ALL) is a type of childhood leukemia with the highest incidence; T-acute lymphocytic leukemia (T-ALL) is far more difficult to treat than B-acute lymphocytic leukemia (B-ALL) and has a poor long-term prognosis. Therefore, there is an urgent requirement to develop effective drugs for the treatment of T-ALL. Hirsutanol A is a natural sesquiterpenoid compound. The aim of the present study was to evaluate the in vitro anticancer activity of hirsutanol A against T-acute lymphocytic leukemia Jurkat cells and investigate the mechanism of action. A Cell Counting Kit-8 assay demonstrated that hirsutanol A inhibited the viability of Jurkat cells in a dose- and time-dependent manner. In addition, hirsutanol A induced cell cycle arrest at the G(2) phase as determined via flow cytometry. Furthermore, Hoechst staining, Annexin V-FITC/propidium iodide double staining, mitochondrial membrane potential detection using JC-1 and western blot analysis of apoptotic proteins indicated that the inhibitory effect of hirsutanol A on Jurkat cells was associated with the induction of apoptosis. Of note, hirsutanol A induced the expression of the tumor suppressor p53, whereas simultaneous treatment with pifithrin-alpha, an inhibitor of p53, significantly reduced Jurkat cell apoptosis induced by hirsutanol A. In summary, the present study suggested that hirsutanol A inhibited Jurkat cell viability through induction of cell cycle arrest and p53-dependent initiation of apoptosis, thus hirsutanol may serve as a promising compound for the treatment of T-ALL.
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