Asahi H, Koshida K, Hori O, Ogawa S, Namiki M
Department of Urology and Third Department of Anatomy, Kanazawa University School of Medicine, Kanazawa, Japan.
BJU Int. 2002 Sep;90(4):462-6. doi: 10.1046/j.1464-410x.2002.02915.x.
To investigate the relationship between the expression of the 150-kDa oxygen-regulated protein (ORP150, which functions as a molecular chaperone in the endoplasmic reticulum for the folding and trafficking of newly synthesized proteins) and the aggressiveness of bladder cancer, and the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs), as the former is a secreting protein through the endoplasmic reticulum and the latter are closely involved in tumour invasion.
Thirty-nine cystectomy specimens, comprising 12 superficial (pT1) and 27 invasive (pT2-pT4) tumours, were immunohistochemically analysed using antibodies against ORP150, VEGF, MMP-1, MMP-2 and MMP-9. Staining was scored from 0 to 3, according to the ratio of positively staining cells.
Staining was positive (score 1-3) for ORP150 in 10 of 12 superficial and 25 (93%) of the invasive tumours, with a significantly higher staining score for stage T4 than stage T1 tumours. The trend was the same for the staining score of MMP-2, and there was a significant correlation between ORP150 and MMP-2 expression.
The expression of ORP150 was common in bladder cancer, with a tendency for greater expression in higher stages. The significant correlation between ORP150 and MMP-2 expression suggests that ORP150 acts as a molecular chaperone for MMP-2 secretion and thus tumour invasion.
研究150kDa氧调节蛋白(ORP150,在内质网中作为分子伴侣参与新合成蛋白质的折叠和运输)的表达与膀胱癌侵袭性之间的关系,以及血管内皮生长因子(VEGF)和基质金属蛋白酶(MMPs)的表达,因为前者是一种通过内质网分泌的蛋白质,而后者与肿瘤侵袭密切相关。
39例膀胱切除术标本,包括12例浅表性(pT1)和27例浸润性(pT2 - pT4)肿瘤,使用抗ORP150、VEGF、MMP - 1、MMP - 2和MMP - 9的抗体进行免疫组织化学分析。根据阳性染色细胞的比例,染色评分为0至3分。
12例浅表性肿瘤中有10例、27例浸润性肿瘤中有25例(93%)的ORP150染色呈阳性(评分1 - 3),T4期肿瘤的染色评分显著高于T1期肿瘤。MMP - 2的染色评分趋势相同,且ORP150与MMP - 2的表达之间存在显著相关性。
ORP150在膀胱癌中表达普遍,且在较高分期中有表达增加的趋势。ORP150与MMP - 2表达之间的显著相关性表明,ORP150作为MMP - 2分泌的分子伴侣,从而促进肿瘤侵袭。