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乳腺癌患者血清的雌激素可逆抑制活性[已修正]

Oestrogen reversible inhibitory activity of sera from breast cancer patients [corrected].

作者信息

Lykkesfeldt A E, Rose C, Thorpe S M, Laursen I, Lykkesfeldt G, Briand P

机构信息

Laboratory of Tumour Endocrinology, Fibiger Institute, Copenhagen, Denmark.

出版信息

Eur J Cancer Clin Oncol. 1988 Oct;24(10):1647-53. doi: 10.1016/0277-5379(88)90058-2.

Abstract

Sera from foetal calves, newborn calves, athymic mice, and healthy postmenopausal women exert a growth inhibitory effect on the oestrogen receptor positive human breast cancer cell line MCF-7. This inhibitory effect of serum can be abrogated by oestradiol. Serum samples from 22 breast cancer patients were analysed for the amount of inhibitory activity in order to clarify whether regulation of cell proliferation of human breast cancer may occur via a modulation of the inhibitory activity in the patient's serum. Twenty of the 22 serum samples showed inhibitory activity and no difference was found in the degree of inhibition. These results do not support the hypothesis that breast cancer cells grow in vivo solely as a function of a reduced level of a serum-borne inhibitory activity; other mechanisms must be involved in the regulation of growth. We have found that MCF-7 cells, the growth of which is inhibited by serum from breast cancer patients, exhibit a reduced synthesis of three secreted proteins, and an increased amount of one protein, a 46K protein. Oestradiol induced cell proliferation is concomitant with stimulation of the synthesis of these three proteins and inhibition of the 46K protein. Regulation of growth of breast cancer may therefore occur via changes in the synthesis of secreted proteins, which exert a regulatory function on cell proliferation.

摘要

来自胎牛、新生牛、无胸腺小鼠和健康绝经后女性的血清对雌激素受体阳性的人乳腺癌细胞系MCF-7具有生长抑制作用。血清的这种抑制作用可被雌二醇消除。分析了22例乳腺癌患者血清样本中的抑制活性量,以阐明人乳腺癌细胞增殖的调节是否可能通过调节患者血清中的抑制活性来实现。22份血清样本中有20份显示出抑制活性,且在抑制程度上未发现差异。这些结果不支持乳腺癌细胞在体内仅作为血清源性抑制活性水平降低的函数而生长的假说;生长调节必定涉及其他机制。我们发现,其生长受到乳腺癌患者血清抑制的MCF-7细胞,三种分泌蛋白的合成减少,而一种46K蛋白的量增加。雌二醇诱导的细胞增殖与这三种蛋白合成的刺激以及46K蛋白的抑制相伴。因此,乳腺癌生长的调节可能通过分泌蛋白合成的变化来实现,这些分泌蛋白对细胞增殖发挥调节功能。

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