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扁柏酚诱导畸胎瘤F9细胞分化。

Hinokitiol induces differentiation of teratocarcinoma F9 cells.

作者信息

Muto N, Dota A, Tanaka T, Itoh N, Okabe M, Inada A, Nakanishi T, Tanaka K

机构信息

Faculty of Pharmaceutical Sciences, Osaka University, Japan.

出版信息

Biol Pharm Bull. 1995 Nov;18(11):1576-9. doi: 10.1248/bpb.18.1576.

DOI:10.1248/bpb.18.1576
PMID:8593483
Abstract

Hinokitiol, a constituent of the wood of Chamaecyparis taiwanensis, was found to induce differentiation of teratocarcinoma F9 cells. When examined by the agar-overlay method, in which expression of plasminogen activator as a differentiation marker protein was detected, this compound exhibited a dose- and time-dependent induction. Induction of differentiation by hinokitiol occurred irreversibly and required its addition for more than 12h. Among its structure-related compounds tested, tropolone and two colchicine-related compounds exerted potent activities comparable to that of hinokitiol. These findings indicate that free tropolone structure in the molecules plays an essential role in inducing differentiation of F9 cells. Hinokitiol showed a strong inhibitory effect of DNA synthesis in very early stages of culture, suggesting that this effect may be responsible for triggering differentiation of F9 cells.

摘要

扁柏酚是台湾扁柏木材的一种成分,已发现其可诱导畸胎癌F9细胞分化。采用琼脂覆盖法检测作为分化标记蛋白的纤溶酶原激活剂的表达时,该化合物呈现出剂量和时间依赖性诱导作用。扁柏酚诱导的分化是不可逆的,且需要添加该化合物超过12小时。在测试的与它结构相关的化合物中,托酚酮和两种与秋水仙碱相关的化合物表现出与扁柏酚相当的强活性。这些发现表明分子中的游离托酚酮结构在诱导F9细胞分化中起重要作用。扁柏酚在培养的早期阶段对DNA合成表现出强烈的抑制作用,表明这种作用可能是触发F9细胞分化的原因。

相似文献

1
Hinokitiol induces differentiation of teratocarcinoma F9 cells.扁柏酚诱导畸胎瘤F9细胞分化。
Biol Pharm Bull. 1995 Nov;18(11):1576-9. doi: 10.1248/bpb.18.1576.
2
Induction of apoptosis by hinokitiol, a potent iron chelator, in teratocarcinoma F9 cells is mediated through the activation of caspase-3.强效铁螯合剂扁柏酚诱导畸胎瘤F9细胞凋亡是通过激活半胱天冬酶-3介导的。
Cell Prolif. 1999 Feb;32(1):63-73. doi: 10.1046/j.1365-2184.1999.3210063.x.
3
Induction of differentiation of embryonal carcinoma F9 cells by iron chelators.铁螯合剂诱导胚胎癌F9细胞分化
Res Commun Mol Pathol Pharmacol. 1995 Nov;90(2):211-20.
4
Apoptosis during iron chelator-induced differentiation in F9 embryonal carcinoma cells.铁螯合剂诱导F9胚胎癌细胞分化过程中的细胞凋亡。
Cell Biol Int. 1999;23(8):541-50. doi: 10.1006/cbir.1999.0407.
5
Hinokitiol suppresses cancer stemness and oncogenicity in glioma stem cells by Nrf2 regulation.扁柏酚通过调控Nrf2抑制胶质瘤干细胞的癌干性和致癌性。
Cancer Chemother Pharmacol. 2017 Aug;80(2):411-419. doi: 10.1007/s00280-017-3381-y. Epub 2017 Jul 6.
6
Reversible effects of sodium butyrate on the differentiation of F9 embryonal carcinoma cells.丁酸钠对F9胚胎癌细胞分化的可逆作用
Exp Cell Res. 1991 Jan;192(1):46-51. doi: 10.1016/0014-4827(91)90155-n.
7
Prooxidant action of hinokitiol: hinokitiol-iron dependent generation of reactive oxygen species.扁柏酚的促氧化作用:扁柏酚-铁依赖的活性氧生成。
Basic Clin Pharmacol Toxicol. 2005 Dec;97(6):392-4. doi: 10.1111/j.1742-7843.2005.pto_214.x.
8
Hinokitiol inhibits compound action potentials in the frog sciatic nerve.桧木醇抑制蛙坐骨神经复合动作电位。
Eur J Pharmacol. 2018 Jan 15;819:254-260. doi: 10.1016/j.ejphar.2017.12.014. Epub 2017 Dec 7.
9
Cytotoxicity of the hinokitiol-related compounds, gamma-thujaplicin and beta-dolabrin.扁柏酚相关化合物γ-崖柏素和β-杜松脑的细胞毒性。
Biol Pharm Bull. 2001 Mar;24(3):299-302. doi: 10.1248/bpb.24.299.
10
Hinokitiol Inhibits Melanogenesis via AKT/mTOR Signaling in B16F10 Mouse Melanoma Cells.双羟萘酸噻嘧啶通过 AKT/mTOR 信号通路抑制 B16F10 小鼠黑素瘤细胞的黑色素生成。
Int J Mol Sci. 2016 Feb 18;17(2):248. doi: 10.3390/ijms17020248.

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New therapeutic strategy of hinokitiol in haemorrhagic shock-induced liver injury.新型桧木醇疗法在失血性休克诱导的肝损伤中的应用。
J Cell Mol Med. 2019 Mar;23(3):1723-1734. doi: 10.1111/jcmm.14070. Epub 2018 Dec 8.
2
Hinokitiol inhibits vasculogenic mimicry activity of breast cancer stem/progenitor cells through proteasome-mediated degradation of epidermal growth factor receptor.扁柏酚通过蛋白酶体介导的表皮生长因子受体降解抑制乳腺癌干细胞/祖细胞的血管生成拟态活性。
Oncol Lett. 2016 Apr;11(4):2934-2940. doi: 10.3892/ol.2016.4300. Epub 2016 Mar 2.
3
Induction of apoptosis by hinokitiol, a potent iron chelator, in teratocarcinoma F9 cells is mediated through the activation of caspase-3.
强效铁螯合剂扁柏酚诱导畸胎瘤F9细胞凋亡是通过激活半胱天冬酶-3介导的。
Cell Prolif. 1999 Feb;32(1):63-73. doi: 10.1046/j.1365-2184.1999.3210063.x.