4.4 Article

Differential expression of kallikrein gene 5 in cancerous and normal testicular tissues

Journal

UROLOGY
Volume 60, Issue 4, Pages 714-718

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/S0090-4295(02)01811-3

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Objectives. Kallikrein gene 5 (KLK5; formerly designated as kallikrein-like gene 2, or human stratum corneum tryptic enzyme) is one of the new members of the human kallikrein gene family on chromosome 19q 13.4. Although it is expressed at low levels in various tissues, KLK5 expression is highest in the human mammary gland and testis. Previous investigations have established that the expression of KLK5 is estrogen and progestin driven in the BT-474 breast cancer cell line. In this study, we focused on KLK5 expression in normal and cancerous testicular tissue. Methods. Fourteen matched testicular tumor and adjacent normal tissue samples were minced on dry ice and homogenized. Total RNA was extracted and mRNA was reverse transcribed. The cDNA samples were amplified by real-time quantitative polymerase chain reaction with KLK5-specific primers to compare the relative KLK5 levels in normal and cancerous testicular tissues. Results. In 13 (93%) of the 14 patients, KLK5 expression in the cancerous area was significantly lower than in the adjacent, histologically confirmed, normal testicular tissue samples (P <0.001). The KLK5 level was 9.0 +/- 3.9 (mean +/- standard error, arbitrary units) in the noncancerous tissue and 4.5 +/- 2.9 in the cancerous tissue. We noted significantly lower KLK5 expression in seminomas than in nonseminomas (P = 0.009), as well as in late-stage (II/III) tumors versus early-stage (I) tumors (P = 0.026). KLK5 expression was also associated with the extent of primary tumor, with tumors with vascular/lymphatic invasion (T2/T3) expressing lower KLK5 message than did tumors limited to the testis and epididymis (T1) (P = 0.008). Conclusions. We found significantly lower expression of KLK5 in testicular tumors than in normal testicular tissue. More studies are necessary to investigate the mechanism behind this finding. (C) 2002, Elsevier Science Inc.

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