scholarly journals In situ androgen producing enzymes in human prostate cancer

2005 ◽  
Vol 12 (1) ◽  
pp. 101-107 ◽  
Author(s):  
Yasuhiro Nakamura ◽  
Takashi Suzuki ◽  
Masao Nakabayashi ◽  
Mareyuki Endoh ◽  
Kazuhiro Sakamoto ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Clinical Stage ◽  
Biological Significance ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
The Status ◽  
Prostate Cancers

Androgens have been proposed to be actively produced in situ in human prostate cancer. These locally produced androgens have also been considered to play important roles in the pathogenesis and development of prostate cancer. Therefore, it is important to examine the status of this in situ androgen metabolism and/or synthesis in detail in order to improve the clinical response to hormonal therapy in patients diagnosed with prostate cancer. Several studies have previously demonstrated the expression of androgen-producing enzymes such as 5α-reductase types 1 and 2, and 17β-hydroxysteroid dehydrogenase type 5 (17β-HSD5), in human prostate carcinoma cells. However, their biological significance has remained largely unknown. In this study, we evaluated the immunoreactivities of these steroidogenic enzymes in human prostate cancer obtained from surgery (n=70), and correlated the findings with clinicopathological features of the patients. 17β-HSD5 immunoreactivity was detected in 54 cases (77%), 5α-reductase type 1 in 51 cases (73%) and 5α-reductase type 2 in 39 cases (56%). 5α-reductase type 2 immunoreactivity was significantly correlated with that of androgen receptor (AR), and 17β-HSD5 positive cases were significantly associated with clinical stage (TNM stage pT3 vs pT2). These data all suggest that androgen-producing enzymes, such as 5α-reductase type 1 and type 2, and 17β-HSD5 are expressed in a majority of prostate cancers, and are involved in the local production and actions of androgens in prostate cancers.

scholarly journals Analytic Validation of RNA In Situ Hybridization (RISH) for AR and AR-V7 Expression in Human Prostate Cancer

2016 ◽  
Vol 22 (18) ◽  
pp. 4651-4663 ◽  
Author(s):  
Liana B. Guedes ◽  
Carlos L. Morais ◽  
Fawaz Almutairi ◽  
Michael C. Haffner ◽  
Qizhi Zheng ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
In Situ Hybridization ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Rna In Situ Hybridization

In situ analysis of N-linked Glycans as Potential Biomarkers of Clinical Course in Human Prostate Cancer

2021 ◽  
pp. molcanres.0967.2020
Author(s):  
Lindsey R Conroy ◽  
Alexandra E Stanback ◽  
Lyndsay E.A Young ◽  
Harrison A Clarke ◽  
Grant L Austin ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Clinical Course ◽  
In Situ Analysis ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Potential Biomarkers

scholarly journals Autocrine Prolactin Promotes Prostate Cancer Cell Growth via Janus Kinase-2-Signal Transducer and Activator of Transcription-5a/b Signaling Pathway

Endocrinology ◽  
2007 ◽  
Vol 148 (7) ◽  
pp. 3089-3101 ◽  
Author(s):  
Ayush Dagvadorj ◽  
Sean Collins ◽  
Jean-Baptiste Jomain ◽  
Junaid Abdulghani ◽  
James Karras ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Signaling Pathway ◽  
Janus Kinase ◽  
Human Prostate ◽  
Signal Transducer ◽  
Human Prostate Cancer ◽  
Janus Kinase 2 ◽  
Prostate Cancer Cells ◽  
Hormone Refractory ◽  
Prostate Cancers

The molecular mechanisms that promote progression of localized prostate cancer to hormone-refractory and disseminated disease are poorly understood. Prolactin (Prl) is a local growth factor produced in high-grade prostate cancer, and exogenously added Prl in tissue or explant cultures of normal and malignant prostate is a strong mitogen and survival factor for prostate epithelium. The key signaling proteins that mediate the biological effects of Prl in prostate cancer are Signal Transducer and Activator of Transcription (Stat)-5a/5b via activation of Janus kinase-2. Importantly, inhibition of Stat5a/b in prostate cancer cells induces apoptotic death. Using a specific Prl receptor antagonist (Δ1–9G129R-hPRL), we demonstrate here for the first time that autocrine Prl in androgen-independent human prostate cancer cells promotes cell viability via Stat5 signaling pathway. Furthermore, we examined a unique clinical material of human hormone refractory prostate cancers and metastases and show that autocrine Prl is expressed in 54% of hormone-refractory clinical human prostate cancers and 62% prostate cancer metastases. Finally, we demonstrate that autocrine Prl is expressed from both the proximal and distal promoters of the Prl gene in clinical human prostate cancers and in vivo and in vitro human prostate cancer models, independently of pituitary transcription factor-1 (Pit-1). Collectively, the data provide novel evidence for the concept that autocrine Prl signaling pathway is involved in growth of hormone-refractory and metastatic prostate cancer. The study also provides support for the use of Prl receptor antagonists or other therapeutic strategies to block the Prl-Janus kinase-2-Stat5 signaling pathway in advanced prostate cancer.

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