脑膜瘤孕激素受体合成与雌激素诱导蛋白pS2和组织蛋白酶D的关系及表皮生长因子、Forskolin和佛波酯的影响。

PubMed ID
发表日期 年月

原始出处 国际生物标记杂志
The International journal of biological markers
作者 Koehorst  S G  Spapens  M E  Van Der Kallen  C J  Van 'T Verlaat  J W  Blaauw  G  Thijssen  J H  Blankenstein  M A 

文献标题 脑膜瘤孕激素受体合成与雌激素诱导蛋白pS2和组织蛋白酶D的关系及表皮生长因子、Forskolin和佛波酯的影响。
Progesterone receptor synthesis in human meningiomas: relation to the estrogen-induced proteins pS2 and cathepsin-D and influence of epidermal growth factor, Forskolin and phorbol ester in vitro.

文献摘要

孕酮受体(PR)在脑膜瘤中的自主表达已被证实。为了评估是否与孕激素受体类似,其他雌激素诱导蛋白也在脑膜瘤中自主表达,我们测定了52例脑膜瘤中pS2和组织蛋白酶D(Cath-D)的浓度。52例脑膜瘤中未检出pS2蛋白。52例脑膜瘤中均可检测到Cath-D蛋白,但脑膜瘤胞浆中Cath-D的平均浓度是54例乳腺肿瘤的2.4倍(p<0.001)。这些结果表明,自主表达是PR相关的而不是雌激素受体相关的现象,因此,雌二醇可能不负责人脑膜瘤PR的合成。为了评估其他非雌二醇依赖性信号通路在PR合成中的作用,我们在体外测试了EGF、Forskolin和phorbol酯对PR合成的影响。在6种不同的原代培养物中加入EGF后,未检测到PR。Forskolin和TPA的加入引起了脑膜瘤细胞的形态学改变,但在两种不同的原发性脑膜瘤培养物中没有诱导PR或pS2的合成。我们的结论是,人脑脑膜瘤中PR的合成不能通过这些生长因子激活的信号通路来触发。


Autonomous expression of progesterone receptors (PR) in human meningiomas is well established. To evaluate whether, similar to progesterone receptors, other estrogen-inducible proteins are also autonomously expressed in meningiomas, concentrations of pS2 and cathepsin-D (Cath-D) were measured in 52 meningiomas. No pS2 protein was detectable in 52/52 tested meningiomas. The Cath-D protein was measurable in all 52 meningiomas, but the mean concentration of Cath-D in meningioma cytosols was 2.4-fold lower than that of a group of 54 breast tumors (p < 0.001). These results indicate that autonomous expression is a PR-related rather than an estrogen receptor-related phenomenon and, consequently, that estradiol is probably not responsible for PR synthesis in human meningiomas. To evaluate the role of other, non-estradiol-dependent signalling pathways in PR synthesis, the effects of EGF, Forskolin and phorbol ester on PR synthesis were tested in vitro. No PR was detectable after the addition of EGF to six different primary cultures. Forskolin and TPA addition caused a morphological change in meningioma cells, but did not induce PR or pS2 synthesis in two different primary meningioma cultures. We conclude that PR synthesis in human meningiomas cannot be triggered by switching on the signalling pathways activated by these growth factors.