Several genes encoding ribosomal proteins are over‐expressed in prostate‐cancer cell lines: Confirmation of L7a and L37 over‐expression in prostate‐cancer tissue samples

A cDNA library specific for mRNA over‐expressed in prostate cancer was generated by subtractive hybridization of transcripts originating from prostatic hyperplasia and cancer tissues. cDNA encoding ribosomal proteins L4, L5, L7a, L23a, L30, L37, S14 and S18 was found to be present among 100 analyzed...

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Veröffentlicht in:International journal of cancer 1998-09, Vol.78 (1), p.27-32
Hauptverfasser: Vaarala, Markku H., Porvari, Katja S., Kyllönen, Atte P., Mustonen, Mika V. J., Lukkarinen, Olavi, Vihko, Pirkko T.
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Sprache:eng
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Zusammenfassung:A cDNA library specific for mRNA over‐expressed in prostate cancer was generated by subtractive hybridization of transcripts originating from prostatic hyperplasia and cancer tissues. cDNA encoding ribosomal proteins L4, L5, L7a, L23a, L30, L37, S14 and S18 was found to be present among 100 analyzed clones. Levels of ribosomal mRNA were significantly higher at least in one of the prostate‐cancer cell lines, LNCaP, DU‐145 and PC‐3, than in hyperplastic tissue, as determined by slot‐blot hybridization. Furthermore, L23a‐ and S14‐transcript levels were significantly elevated in PC‐3 cells as compared with those in the normal prostate epithelial cell line PrEC. Generally, dramatic changes in the mRNA content of the ribosomal proteins were not detected, the most evident over‐expression being that of L37 mRNA, which was 3.4 times more abundant in LNCaP cells than in hyperplastic prostate tissue. The over‐expression of L7a and L37 mRNA was confirmed in prostate‐cancer tissue samples by in situ hybridization. Elevated cancer‐related expression of L4 and L30 has not been reported, but levels of the other ribosomal proteins are known to be increased in several types of cancers. These results therefore suggest that prostate cancer is comparable with other types of cancers, in that a larger pool of some ribosomal proteins is gained during the transformation process, by an unknown mechanism. Int. J. Cancer 78:27–32, 1998.© 1998 Wiley‐Liss, Inc.
ISSN:0020-7136
1097-0215
DOI:10.1002/(SICI)1097-0215(19980925)78:1<27::AID-IJC6>3.0.CO;2-Z