- Tytuł:
- Comparative analysis of prostatic acid phosphatase and prostate-specific antigen mRNA levels in hyperplastic prostate stimulated with steroid hormones and growth factors.
- Autorzy:
-
Dulińska, Joanna
Laidler, Piotr
Łabędź, Maria - Powiązania:
- https://bibliotekanauki.pl/articles/1043762.pdf
- Data publikacji:
- 2002
- Wydawca:
- Polskie Towarzystwo Biochemiczne
- Tematy:
-
hyperplastic prostate
prostate-specific antigen
androgens
growth factors
prostatic acid phosphatase - Opis:
- Prostatic acid phosphatase (PAP) and prostate-specific antigen (PSA) are the markers of human prostatic gland. However, it is still not completely understood if and how, steroid hormones and growth factors affect their expression and metabolism in the respect to the major pathologies of the gland. Appropriate studies were carried out on histopathologically diagnosed benign prostatic hyperplasia - BPH (n = 42) using tissue slices and cells derived from them. They were incubated with steroid hormones: 5-α-dihydrotestosterone (DHT), estradiol (E) and growth factors: epidermal growth factor (EGF), basic fibroblastic growth factor (bFGF) under culture conditions for up to 24 hours. 32P-labelled specific oligonucleotide probes were used to analyze total RNA isolated from each sample for the presence of PAP and PSA mRNAs. DHT, E, bFGF, EGF or both DHT + bFGF and DHT + EGF increased PAP and PSA mRNA levels in a time- and dose-dependent manner. The highest and statistically significant increase (P <0.001) for PAP mRNA was observed when DHT + bFGF were present in the medium while for PSA mRNA if DHT + EGF were added to the medium. Slow but constant decrease of PAP and PSA mRNA levels was observed in the absence of each of these factors in the incubation medium. The results suggest that early expression of PSA and PAP genes and/or their mRNA stability strongly depend on DHT while differ in their response to EGF and bFGF.
- Źródło:
-
Acta Biochimica Polonica; 2002, 49, 2; 357-368
0001-527X - Pojawia się w:
- Acta Biochimica Polonica
- Dostawca treści:
- Biblioteka Nauki
Artykuł