DIFFERENT EXPRESSION PATTERNS OF SOMATOSTATIN RECEPTOR SUBTYPES IN CULTURED EPITHELIAL-CELLS FROM HUMAN NORMAL PROSTATE AND PROSTATE-CANCER

Citation
Aa. Sinisi et al., DIFFERENT EXPRESSION PATTERNS OF SOMATOSTATIN RECEPTOR SUBTYPES IN CULTURED EPITHELIAL-CELLS FROM HUMAN NORMAL PROSTATE AND PROSTATE-CANCER, The Journal of clinical endocrinology and metabolism, 82(8), 1997, pp. 2566-2569
Citations number
25
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
82
Issue
8
Year of publication
1997
Pages
2566 - 2569
Database
ISI
SICI code
0021-972X(1997)82:8<2566:DEPOSR>2.0.ZU;2-Q
Abstract
The transcripts of five SRIH receptor subtypes (SSTR1, SSTR2, SSTR3, S STR4, and SSTR5) were investigated by RT-PCR in epithelial cells (EC) and stromal cells (SC) from primary cultures of five normal human pros tates and six prostate cancers. Primary cultures of prostate EC were e stablished in serum-free keratinocyte medium with 5% FCS, epidermal gr owth factor, and bovine pituitary extract; SC were cultured in MEM wit h 10% FCS. Total RNA was extracted from EC and SC using a modified gua nidine thiocyanate method. RT-PCR was performed after deoxyribonucleas e treatment, using SSTR1-, SSTR2- SSTR3-, SSTR4-, and SSTR5-specific p rimers and adding glyceraldehyde-3-phosphate dehydrogenase-specific pr imers as internal control. A PCR product of the expected size of 334 b p, corresponding to SSTR1. was expressed only in EC from prostate canc er, whereas the expected 461-bp product of SSTR2 was found only in EC from normal prostate. SSTR3 messenger RNA was undetectable in not mal and cancer EC, whereas SSTR4 and SSTR5 were present in both cell types . SSTR1, SSTR2, SSTR3, SSTR4, and SSTR5 messenger RNAs were not expres sed in SC from both normal and cancer prostates, The RT-PCR method cle arly demonstrated SSTRs' expression in the human prostate EC in vitro with differences between normal and tumoral samples. Our results may e xplain the ineffectiveness of some SSTR2 selective SRIH analogues in t he treatment of prostate cancer and suggest that the absence of SSTR2 could represent a growth advantage in prostate cancer.