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Cyclin D1 expression in human prostate carcinoma cell lines and primary tumors
Author(s) -
Han Edward KyuHo,
Lim Jin T.E.,
Arber Nadir,
Rubin Mark A.,
Xing Wang Qiu,
Weinstein I. Bernard
Publication year - 1998
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19980501)35:2<95::aid-pros2>3.0.co;2-f
Subject(s) - cyclin d1 , prostate cancer , prostate , cancer research , cyclin d , cancer , biology , pca3 , cyclin b , pathology , medicine , cell cycle , genetics
BACKGROUND The cyclin D1 gene is amplified and/or overexpressed in several types of human cancer, including cancers of the breast, esophagus, head, and neck. However, the role of cyclin D1 in prostate cancer has not been previously studied in detail. METHODS Six human prostate cancer cell lines and cultures of normal human prostate cells were examined by Western and Northern blot analyses for levels of expression of the cyclin D1 protein and mRNA, respectively. Southern blot analyses were performed to examine possible amplification of this gene. Immunostaining for cyclin D1 was performed on 50 primary prostate cancer samples. RESULTS Cyclin D1 protein was expressed at relatively high levels in all of the six human prostate cancer cell lines examined, but was not detected in the cultures of normal human prostate cells. The ALVA 41 cell line expressed the highest level of this protein. Relatively high levels of cyclin D1 mRNA were also found in all of the prostate cancer cell lines. Nevertheless, none of these cell lines revealed amplification of the cyclin D1 gene. Twelve of the 50 primary prostate cancer samples (24%) revealed regions of moderate to strongly positive staining for cyclin D1. CONCLUSIONS The increased expression of cyclin D1 in several prostate cancer cell lines and in a subset of primary prostate cancer samples suggests that further studies on the expression of this gene and related genes may be of interest in understanding the pathogenesis of prostate cancer. Prostate 35:95–101, 1998. © 1998 Wiley‐Liss, Inc.