Kim I Y, Ahn H J, Zelner D J, Shaw J W, Lang S, Kato M, Oefelein M G, Miyazono K, Nemeth J A, Kozlowski J M, Lee C
Department of Urology, Northwestern University Medical School, Chicago, Illinois 60611, USA.
Clin Cancer Res. 1996 Aug;2(8):1255-61.
Transforming growth factor beta1 (TGF-beta1) is a potential regulator of prostate cancer cell growth that signals through a heteromeric complex composed of type I and type II receptors. In the present study, an attempt was made to establish a correlation between expression of TGF-beta receptors and tumor grade in archival human prostate cancer tissues. To this end, immunohistochemical studies for TGF-beta receptors were carried out on 32 cases of human prostate cancer and 8 samples of benign human prostate. In both benign and malignant human prostate tissues, immunoreactivity for both type I and type II receptors was detected predominantly in epithelial cells. In addition, there was an inverse correlation between the loss of expression of TGF-beta1 type I and type II receptors and the tumor grade. Of the 32 prostate cancer cases screened, staining was completely absent in four samples for type II receptor (P < 0.05) and eight samples for type I receptor (P < 0.025). In contrast, all eight samples of benign prostate tissues investigated in this study showed strong staining for both type I and type II receptors. These results, taken together, indicate that human prostate cancer cells frequently have loss of expression of TGF-beta type I and/or type II receptors. Furthermore, these observations provide a potential mechanism for prostate cancer cells to escape the growth-inhibitory effect of TGF-beta.
转化生长因子β1(TGF-β1)是前列腺癌细胞生长的潜在调节因子,它通过由I型和II型受体组成的异源复合物发出信号。在本研究中,试图在存档的人类前列腺癌组织中建立TGF-β受体表达与肿瘤分级之间的相关性。为此,对32例人类前列腺癌和8例良性人类前列腺样本进行了TGF-β受体的免疫组织化学研究。在良性和恶性人类前列腺组织中,I型和II型受体的免疫反应性主要在上皮细胞中检测到。此外,TGF-β1 I型和II型受体表达的缺失与肿瘤分级呈负相关。在筛查的32例前列腺癌病例中,II型受体的四个样本和I型受体的八个样本完全没有染色(P < 0.05和P < 0.025)。相比之下,本研究中调查的所有八个良性前列腺组织样本对I型和II型受体均显示出强染色。综上所述,这些结果表明人类前列腺癌细胞经常出现TGF-β I型和/或II型受体表达缺失。此外,这些观察结果为前列腺癌细胞逃避TGF-β的生长抑制作用提供了一种潜在机制。