Applications
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In HL-60 cells, HA14-1 induced cell death in a dose-dependent manner. HA14-1 (50 μM) caused the loss of viability in more than 90% of the cells. In HL-60 cells, treatment with 50 μM HA14-1 by 3 h displayed the characteristic pattern of DNA fragmentation. HA14-1 decreased cell viability and induced apoptosis in follicular lymphoma B cell lines, HF1A3, HF4.9 and HF28RA cells. HA14-1 (10-20 μmol/L) increased sensitivity of human glioblastoma cells to radiotherapy-induced apoptosis and chemotherapy-induced apoptosis.
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Application
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In Swiss nude mice challenged with BeGBM cells, HA14-1 (400 nmol, once weekly from day 2) did not have any significant effect on the growth of glioblastoma tumors in immunodeficient mice. HA14-1 (400 nM) increased the effect of the DNA-damaging agent etoposide (2.5 mg/kg) on glioblastoma growth in vivo.
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References:
[1]. Wang J L, Liu D, Zhang Z J, et al. Structure-based discovery of an organic compound that binds Bcl-2 protein and induces apoptosis of tumor cells[J]. Proceedings of the National Academy of Sciences, 2000, 97(13): 7124-7129.
[2]. Skommer J, Wlodkowic D, Mtt M, et al. HA14-1, a small molecule Bcl-2 antagonist, induces apoptosis and modulates action of selected anticancer drugs in follicular lymphoma B cells[J]. Leukemia research, 2006, 30(3): 322-331.
[3]. Manero F, Gautier F, Gallenne T, et al. The small organic compound HA14-1 prevents Bcl-2 interaction with Bax to sensitize malignant glioma cells to induction of cell death[J]. Cancer research, 2006, 66(5): 2757-2764.
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