反义TR3孤儿受体在依托泊苷治疗时可提高前列腺癌细胞的活力。
Antisense TR3 orphan receptor can increase prostate cancer cell viability with etoposide treatment.
作者信息
Uemura H, Chang C
机构信息
George Whipple Laboratory for Cancer Research, Department of Pathology, University of Rochester, New York 14642, USA.
出版信息
Endocrinology. 1998 May;139(5):2329-34. doi: 10.1210/endo.139.5.5969.
In androgen-responsive LNCaP human prostatic cancer cells, human TR3 orphan receptor, a member of the steroid receptor superfamily, can be rapidly induced by androgen. In contrast, ablation of androgen by castration can induce the expression of the TR3 orphan receptor gene in rat ventral prostate that has undergone apoptosis. This phenomenon prompted us to further analyze the potential role of human TR3 orphan receptor in prostate cancer cells in which apoptosis had been induced. Northern blot analysis shows that human TR3 orphan receptor expression can be induced rapidly after treatment of LNCaP and PC-3 prostate cancer cells with calcium ionophore or etoposide. Our data further demonstrate that a much higher concentration of etoposide was needed to kill the same number of cells in LNCaP and PC-3 cells transfected stably with antisense TR3 orphan receptor compared with that in control vector transfectants. Together, our data suggest that the human TR3 orphan receptor may play an important role in modulating drug-induced prostate apoptosis.
在雄激素应答性LNCaP人前列腺癌细胞中，人TR3孤儿受体作为类固醇受体超家族的一员，可被雄激素迅速诱导。相反，通过去势去除雄激素可诱导已发生凋亡的大鼠腹侧前列腺中TR3孤儿受体基因的表达。这一现象促使我们进一步分析人TR3孤儿受体在已诱导凋亡的前列腺癌细胞中的潜在作用。Northern印迹分析表明，用钙离子载体或依托泊苷处理LNCaP和PC-3前列腺癌细胞后，人TR3孤儿受体的表达可迅速被诱导。我们的数据进一步证明，与对照载体转染细胞相比，用反义TR3孤儿受体稳定转染的LNCaP和PC-3细胞需要更高浓度的依托泊苷才能杀死相同数量的细胞。总之，我们的数据表明人TR3孤儿受体可能在调节药物诱导的前列腺细胞凋亡中起重要作用。
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