scholarly journals KLK4T2 Is a Hormonally Regulated Transcript from the KLK4 Locus

2021 ◽  
Vol 22 (23) ◽  
pp. 13023
Author(s):  
Åke Lundwall ◽  
Erik Bovinder Ylitalo ◽  
Pernilla Wikström ◽  
Maria Brattsand
Keyword(s):  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Prostate Cancer Cell ◽  
Cell Extract ◽  
Prostatic Hyperplasia ◽  
Regulatory Function ◽  
Translation Product ◽  
Intracellular Protein ◽  
Prostate Cancer Cell Lines ◽  
Primary Prostate Cancer

The human kallikrein-related peptidase 4 (KLK4) and the transcribed pseudogene KLKP1 are reported to be highly expressed in the prostate. When trying to clone transcripts of KLKP1, we partly failed. Instead, we identified an androgen-regulated transcript, KLK4T2, which appeared to be a splice variant of KLK4 that also contained exons of KLKP1. Expression analysis of KLK4, KLK4T2, and KLKP1 transcripts in prostate cancer cell lines showed high levels of KLKP1 transcripts in the nucleus and in unfractionated cell extract, whereas it was almost completely absent in the cytoplasmatic fraction. This was in contrast to KLK4 and KLK4T2, which displayed high to moderate levels in the cytoplasm. In patient cohorts we found significantly higher expression of both KLK4T2 and KLK4 in benign prostatic hyperplasia compared to both primary prostate cancer and bone metastasis. Analysis of tissue panels demonstrated the highest expression of KLK4T2 in the prostate, but in contrast to the classical KLK4, relatively high levels were also found in placenta. So far, the function of KLK4T2 is still to be explored, but the structure of the translation product indicated that it generates a 17.4 kDa intracellular protein with possible regulatory function.

scholarly journals Benign prostatic hyperplasia (BPH) epithelial cell line BPH-1 induces aromatase expression in prostatic stromal cells via prostaglandin E2

2007 ◽  
Vol 195 (1) ◽  
pp. 89-94 ◽  
Author(s):  
Quan Wu ◽  
Ying Zhou ◽  
Linfeng Chen ◽  
Jiandang Shi ◽  
Chun-Yu Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Epithelial Cell ◽  
Stromal Cells ◽  
Prostate Cancer Cell ◽  
Prostatic Hyperplasia ◽  
Epithelial Cell Line ◽  
Prostate Cancer Cell Lines ◽  
Aromatase Expression ◽  
Cox 2

Estradiol (E2) level in stroma of benign prostatic hyperplasia (BPH) increases with age, and this increase was associated with an elevated expression of aromatase in prostatic stromal cells (PrSCs). Here, we showed that conditioned medium (CM) of BPH-1 (a benign hyperplastic prostatic epithelial cell line), but not of prostate cancer cell lines (LNCaP, DU-145, and PC-3), stimulates aromatase expression in PrSCs. Cyclooxygenase-2 (COX-2) mRNA level in BPH-1, as well as prostaglandin E2 (PGE2) concentration in BPH-1 CM, was significantly higher than that of prostate cancer cell lines. CM of BPH-1 treated with NS-398 (a specific inhibitor of COX-2) failed to stimulate aromatase expression in PrSCs. And PGE2 can stimulate aromatase expression in PrSCs. Our data suggested that BPH-1 induced aromatase expression in PrSCs through the production of PGE2 in a paracrine mechanism.

Differential expression of neutral endopeptidase-24.11 (neprilysin) and endothelin-converting enzyme in human prostate cancer cell lines

2002 ◽  
Vol 103 (s2002) ◽  
pp. 314S-317S ◽  
Author(s):  
Badar A. USMANI ◽  
Ben HARDEN ◽  
Norman J. MAITLAND ◽  
Anthony J. TURNER
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cell Lines ◽  
Prostate Cancer Cell ◽  
Neutral Endopeptidase ◽  
Prostatic Hyperplasia ◽  
Converting Enzyme ◽  
Prostate Cancer Cell Lines ◽  
Endothelin Converting Enzyme ◽  
Androgen Independent

Neutral endopeptidase-24.11 (neprilysin; NEP/CD10) is a cell surface metallopeptidase expressed by prostatic epithelial cells that degrades various bioactive peptides including endothelin. Endothelin-converting enzyme (ECE), the key enzyme of endothelin biosynthesis, catalyses the final processing step in the pathway. Neuropeptide substrates of NEP, including endothelin, have been implicated in the growth of androgen-independent prostate cancer. We have surveyed the expression of NEP and ECE in a range of prostate cancer cell lines. Western analysis reveals that ECE-1 is expressed abundantly in all the malignant cell lines tested, except for LNCaP. In contrast, LNCaP cells express high levels of NEP, while NEP was not detected in PC-3, DU145 and other metastatic cell lines that were tested. Of the normal immortalized prostate epithelial cell lines, PNT1a shows equivalent amounts of NEP and ECE. PNT2-C2 shows poor NEP expression but an abundance of ECE. P4E6, by comparison, has low levels of both ECE and NEP. These differences in expression may render these cell lines useful in experimental models for future study. Benign prostatic hyperplasia primary epithelial cells express much higher levels of NEP than malignant primary epithelial cells, but neither show ECE expression. On the other hand, surrounding stromal cell populations have detectable ECE levels. An absence of ECE in malignant and benign prostatic hyperplasia cells of primary epithelial origin suggests an important role for stromal interaction and paracrine production of ECE within the host. The upregulation of ECE expression in metastatic cells in culture may be indicative of its role in metastatic progression. A differential profile of ECE and NEP could contribute to an abundance of mitogenic peptides aiding the progression of androgen-independent prostate cancer.

scholarly journals Androgen receptor isoforms expression in benign prostatic hyperplasia and primary prostate cancer

PLoS ONE ◽  
2018 ◽  
Vol 13 (7) ◽  
pp. e0200613 ◽  
Author(s):  
Ana Caroline Hillebrand ◽  
Lolita Schneider Pizzolato ◽  
Brasil Silva Neto ◽  
Gisele Branchini ◽  
Ilma Simoni Brum
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Benign Prostatic Hyperplasia ◽  
Prostatic Hyperplasia ◽  
Receptor Isoforms ◽  
Primary Prostate Cancer

Free and complexed prostate-specific antigen serum ratios to predict probability of primary prostate cancer and benign prostatic hyperplasia

Urology ◽  
1996 ◽  
Vol 48 (6) ◽  
pp. 16-22 ◽  
Author(s):  
Garry M. Marley ◽  
M. Craig Miller ◽  
Michael W. Kattan ◽  
Gang Zhao ◽  
Kevin P. Patton ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Benign Prostatic Hyperplasia ◽  
Prostate Specific Antigen ◽  
Specific Antigen ◽  
Prostatic Hyperplasia ◽  
Primary Prostate Cancer
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