A COMPARATIVE-STUDY ON EXPRESSION OF PROSTATIC INHIBIN PEPTIDE, PROSTATE ACID-PHOSPHATASE AND PROSTATE-SPECIFIC ANTIGEN IN ANDROGEN-INDEPENDENT HUMAN AND RAT PROSTATE CARCINOMA CELL-LINES

Citation
Sv. Garde et al., A COMPARATIVE-STUDY ON EXPRESSION OF PROSTATIC INHIBIN PEPTIDE, PROSTATE ACID-PHOSPHATASE AND PROSTATE-SPECIFIC ANTIGEN IN ANDROGEN-INDEPENDENT HUMAN AND RAT PROSTATE CARCINOMA CELL-LINES, Cancer letters, 70(3), 1993, pp. 159-166
Citations number
34
Categorie Soggetti
Oncology
Journal title
ISSN journal
03043835
Volume
70
Issue
3
Year of publication
1993
Pages
159 - 166
Database
ISI
SICI code
0304-3835(1993)70:3<159:ACOEOP>2.0.ZU;2-3
Abstract
Prostatic inhibin peptide (PIP), consisting of 94 amino-acid residues is synthesized and secreted by the prostate gland. Previous studies on immunohistochemical localization of PIP in primary prostatic tumor an d their metastasis, have documented the value of this peptide as a tum or marker for diagnosis of prostate cancer (PCa). The present study wa s undertaken to compare the expression of PIP with that of prostate sp ecific antigen (PSA) and prostatic acid phosphatase (PAP) in androgen independent human PCa cell lines (PC-3, DU-145 and TSU-Prl) by immunop eroxidase technique. The results of the study indicated that the stain ing for PIP was more intense than that of PSA and PAP. The PSA stainin g was either weakly positive (PC-3) or totally absent (TSU-Prl and DU- 145) while PAP staining was intense in PC-3 and moderate in the other two human cell lines. The intense staining observed for PIP in all of the androgen independent cell lines suggests that the synthesis and se cretion of PIP is not primarily dependent on androgens. Furthermore, e xpression of these markers in Dunning rat,cultured adenocarcinoma cell lines and tumors were studied. Positive staining for all three human tumor associated antigens (PIP, PSA and PAP) cross-reacting with the D unning rat PCa cell lines and the tumors, suggest the suitability of t his model for preclinical screening of various therapeutic agents.