Increased Expression of High Mobility Group Protein I(Y) in High Grade Prostatic Cancer Determined by in Situ Hybridization

Yahya Tamimi, Henk G. van der Poel, H. Rainy Umbas, Frans M.J. Debruyne, Jack A. Schalken

Research output: Contribution to journalArticlepeer-review

144 Citations (Scopus)

Abstract

In a previous study using the Dunning rat prostate cancer model, we found high mobility group protein I-(Y) [HMG-IOO] to be overexpressed in metastatic tumor lines when compared to nonmetastatic lines. Hence, overexpression of this 12-kDa non-histone chromosomal protein may be associated with tumor progression. Firstly, by Northern analysis we showed that HMG-I(Y) expression increases in high grade prostate tumors. These studies, however, required fresh material, and clinical follow-up was limited. To overcome this problem paraffin-embedded material must be made amenable for determination of HMG-I(Y) expression in retrospective studies. RNA in situ hybridization enables the evaluation of mRNA levels in such material. We studied tumors from 71 patients with prostate cancer. The microscopic analysis of each sample included: (a) hybridization on sections with sense HMG-I(Y) and (b) 28S rRNA probes (nonspecific signal); (c) hybridization with antisense 28S rRNA (RNA preservation); (d) hybridization with an antisense HMG-I(Y) probe [quantification of HMG-I(Y) mRNA in the expressing areas]. Data were quantified using an image analysis system. High expression of HMG-I(Y) was observed in regions with high Gleason grade (4 and 5); whereas in lesions of Gleason grade 3, both weak and no expression was observed. In areas of grade 1 and 2, as well as in normal glands, low or no expression was found. We conclude that HMG-I(Y) expression assessed by RNA in situ hybridization is related to tumor differentiation in prostate cancer. These findings indicate that HMG-I(Y) expression may be a marker in prostate cancer diagnosis, and the possible clinical implication of expression of this gene in malignancy is discussed in this report. 1 This work was supported by Dutch Cancer Foundation NUKC 9001 and FUSEX (Y.T).2 To whom requests for reprints should be addressed, at UrologicaJ Research Laboratory, University Hospital Nijmegen, P. O. Box 9101,6500HB Nijmegen, the Netherlands.

Original languageEnglish
Pages (from-to)5512-5516
Number of pages5
JournalCancer Research
Volume53
Issue number22
Publication statusPublished - 15 Nov 1993

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