Suppr超能文献

人正常组织和肿瘤组织中冯·希佩尔-林道基因产物的免疫染色

Immunostaining of the von Hippel-Lindau gene product in normal and neoplastic human tissues.

作者信息

Corless C L, Kibel A S, Iliopoulos O, Kaelin W G

机构信息

Department of Pathology, Oregon Health Sciences University, Portland, USA.

出版信息

Hum Pathol. 1997 Apr;28(4):459-64. doi: 10.1016/s0046-8177(97)90035-6.

Abstract

Alterations in the von Hippel-Lindau (VHL) gene are correlated with a diverse group of neoplasms including hemangioblastoma, clear cell renal carcinoma (RCC), and pheochromocytoma. Molecular genetic studies suggest that VHL is a tumor-suppressor gene; correspondingly, reintroduction of a VHL complementary DNA (cDNA) into RCC cells inhibits their ability to form tumors in nude mice. Recently, it was discovered that the VHL gene product (pVHL) binds to two subunits of the transcription elongation complex Elongin (SIII), resulting in decreased activity of this complex in vitro. It is proposed that pVHL functions in vivo as a negative regulator of transcription elongation; however, the intracellular localization of pVHL has not been clearly delineated. Epitope-tagged pVHL has been observed in either the nucleus or the cytoplasm of cultured cells, depending on the density of the cell culture. In this article, the cellular localization of pVHL in normal and neoplastic human tissues is documented using three different monoclonal antibodies. Strong expression of pVHL was observed in the epithelial cells of all organs examined, particularly in renal tubules, and was exclusively cytoplasmic. Lesser degrees of staining, also cytoplasmic, were observed in other cell types. A variety of carcinomas (lung, prostate, colon, breast, bladder, and thyroid) showed strong cytoplasmic staining for pVHL including four of five sporadic clear cell RCC. Of the nonepithelial neoplasms examined, only one tumor, an embryonal rhabdomyosarcoma, failed to stain for pVHL. The findings establish wide-spread expression of VHL at the protein level and provide strong evidence that most, if not all, pVHL is localized to the cytoplasm of cells in vivo.

摘要

冯·希佩尔-林道(VHL)基因的改变与多种肿瘤相关,包括成血管细胞瘤、透明细胞肾细胞癌(RCC)和嗜铬细胞瘤。分子遗传学研究表明VHL是一种肿瘤抑制基因;相应地,将VHL互补DNA(cDNA)重新导入RCC细胞可抑制其在裸鼠体内形成肿瘤的能力。最近,发现VHL基因产物(pVHL)与转录延伸复合物延伸素(SIII)的两个亚基结合,导致该复合物在体外活性降低。有人提出pVHL在体内作为转录延伸的负调节因子发挥作用;然而,pVHL的细胞内定位尚未明确界定。根据细胞培养的密度,在培养细胞的细胞核或细胞质中都观察到了表位标记的pVHL。在本文中,使用三种不同的单克隆抗体记录了pVHL在正常和肿瘤性人类组织中的细胞定位。在所有检查的器官上皮细胞中均观察到pVHL的强表达,尤其是在肾小管中,且仅位于细胞质中。在其他细胞类型中也观察到程度较轻的染色,同样位于细胞质中。多种癌(肺癌、前列腺癌、结肠癌、乳腺癌、膀胱癌和甲状腺癌)对pVHL显示出强细胞质染色,包括五例散发性透明细胞RCC中的四例。在所检查的非上皮性肿瘤中,只有一种肿瘤,即胚胎性横纹肌肉瘤,未对pVHL染色。这些发现确立了VHL在蛋白质水平上的广泛表达,并提供了有力证据,表明在体内大多数(如果不是全部)pVHL定位于细胞的细胞质中。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验