| Autor: |
Tong ZG; Department of General Surgery, Fourth Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, China., Liu N; Department of Pathology, First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, China., Song HS; Department of Pathology, First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, China., Li JQ; Department of Pathology, First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, China., Jiang J; Department of Pathology, First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, China., Zhu JY; Department of Pathology, First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, China., Qi JP; Department of Pathology, First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, China 252302504@qq.com. |
| Abstrakt: |
Cytochalasin B (CB) is known to inhibit a number of cancer types, but its effects on gliomas are unknown. We examined the in vitro effects of CB on the proliferation of human glioma U251 cells, as well as determined its mechanism of action. Cell proliferation was determined using CCK-8. The effect of CB on U251 cell morphology was observed under a transmission electron microscope. Cell cycle distribution was assessed using propidium iodine and Giemsa staining, and cell apoptosis was determined by annexin V-fluorescein isothiocyanate/propidium iodide. Cell cycle-related proteins were determined by Western blot. CB effectively inhibited U251 cell proliferation in a dose- and time-dependent manner. The 24, 48, 72, and 96 h IC50 values were 6.41 x 10(-2), 9.76 x 10(-4), 2.57 x 10(-5), and 2.08 x 10(-5) M, respectively. CB increased the proportion of cells in the G2/M phase in a dose-dependent manner, thus increasing the mitotic index and decreasing cdc2 and cyclin B1 protein levels. CB induced morphological changes in the cytoskeleton. Additionally, 10(-5) M CB induced apoptosis in 23.4 ± 0.5% of U251 cells (P < 0.05 vs control group). Caspase-3, -8, and -9 activities were increased after CB treatment. CB inhibited U251 glioma cell proliferation by damaging the microfilament structure. CB also induced glioma cell apoptosis, suggesting that it may be an effective therapeutic agent against gliomas. |
