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Fas对PC-3和LNCAP前列腺癌细胞系生长及凋亡反应的调节作用

Modulation of growth and apoptosis response in PC-3 and LNCAP prostate-cancer cell lines by Fas.

作者信息

Takeuchi T, Sasaki Y, Ueki T, Kaziwara T, Moriyama N, Kawabe K, Kakizoe T

机构信息

Department of Urology, Faculty of Medicine, University of Tokyo, Japan.

出版信息

Int J Cancer. 1996 Sep 4;67(5):709-14. doi: 10.1002/(SICI)1097-0215(19960904)67:5<709::AID-IJC20>3.0.CO;2-Z.

DOI:10.1002/(SICI)1097-0215(19960904)67:5<709::AID-IJC20>3.0.CO;2-Z
PMID:8782663
Abstract

Fas/APO-1 is a cell-surface protein, a member of the TNF-receptor family, and it potentially induces apoptosis. In presence of an apoptosis-inducible anti-human Fas MAb, Fas-negative control PC-3 human prostate-cancer cells did not undergo morphological changes, while PC-3 human Fas transfectants showed apoptotic changes in vitro. However, LNCaP human Fas transfectants, as well as Fas-negative control LNCaP human prostate-cancer cells, were Fas-resistant. The growth of Fas-transfected PC-3 tumor was retarded compared with that of control PC-3 tumor in vivo without stimulation of anti-human Fas MAb. Anti-human Fas MAb administration in vivo caused macroscopic Fas-transfected PC-3 tumors formed in BALB/c nude mice to undergo apoptosis.

摘要

Fas/APO-1是一种细胞表面蛋白,属于肿瘤坏死因子受体家族成员,具有潜在诱导细胞凋亡的作用。在存在可诱导细胞凋亡的抗人Fas单克隆抗体的情况下,Fas阴性对照的PC-3人前列腺癌细胞未发生形态学改变,而PC-3人Fas转染细胞在体外呈现出凋亡变化。然而,LNCaP人Fas转染细胞以及Fas阴性对照的LNCaP人前列腺癌细胞对Fas具有抗性。在体内未用抗人Fas单克隆抗体刺激的情况下,与对照PC-3肿瘤相比,Fas转染的PC-3肿瘤生长受到抑制。在体内给予抗人Fas单克隆抗体可使BALB/c裸鼠体内形成的宏观Fas转染PC-3肿瘤发生凋亡。

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Essential role for hematopoietic Fas ligand (FasL) in the suppression of melanoma lung metastasis revealed in bone marrow chimeric mice.骨髓嵌合小鼠中揭示造血细胞Fas配体(FasL)在抑制黑色素瘤肺转移中的重要作用。
Clin Exp Metastasis. 2004;21(3):251-6. doi: 10.1023/b:clin.0000037727.28386.4e.
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Resistance to apoptosis induced by microenvironmental stresses is correlated with metastatic potential in Lewis lung carcinoma.
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Fas and Fas ligand interactions suppress melanoma lung metastasis.Fas与Fas配体的相互作用可抑制黑色素瘤肺转移。
J Exp Med. 1998 Nov 2;188(9):1717-23. doi: 10.1084/jem.188.9.1717.