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Cell lines
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HeLa, Vero, L, HEp2, and MDBK cells, SC-1 cells, Murine CT26 colorectal carcinoma cells
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Applications
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In HeLa, Vero, L, HEp2, and MDBK cells, cytochalasin D (0.2-0.5 μg/mL) induced sustained contraction (contracture), loss of microvilli, expression of endoplasmic contents (zeiosis), nuclear protrusion, and extension of cytoplasmic processes. Cells in G1 were most sensitive to CD; responsiveness decreased progressively during early S and is least in mid S through G2. CD inhibited transport of [14C]deoxyglucose in HeLa. In SC-1 cells, Cytochalasin D treatment severely disrupted network organization, increased the number of actin filament ends, and led to the formation of filamentous aggregates or foci composed mainly of actin filaments. Cytochalasin D (0.24-15 μg/mL, 16 h) inhibited CT26 tumor cell proliferation in time and dose dependent manner and induced significant CT26 cell apoptosis.
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Application
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Cytochalasin D (i.v., 50 mg/kg) in vivo treatment significantly inhibited tumor growth and prolonged the survival times in CT26 tumor-bearing mice. In porcine coronary model, Cytochalasin D (2 μg) resulted in less late lumen loss in low-dose. High-dose Cytochalasin D (20 μg) inhibited both late lumen loss and intimal area.
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References:
[1] Miranda A F, Godman G C, Deitch A D, et al. Action of cytochalasin D on cells of established lines [J]. The Journal of cell biology, 1974, 61 (2): 481-500.
[2] Schliwa M. Action of cytochalasin D on cytoskeletal networks[J]. The Journal of cell biology, 1982, 92 (1): 79-91.
[3] Huang F Y, Li Y N, Mei W L, et al. Cytochalasin D, a tropical fungal metabolite, inhibits CT26 tumor growth and angiogenesis[J]. Asian Pacific journal of tropical medicine, 2012, 5 (3): 169-174.
[4].Salu K J, Bosmans J M, Huang Y, et al. Effects of cytochalasin D-eluting stents on intimal hyperplasia in a porcine coronary artery model [J]. Cardiovascular research, 2006, 69 (2): 536-544.
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