Benign prostatic hyperplasia (BPH) is a chronic proliferative disease showing stromal-dominant proliferation. However, the detailed proliferation mechanism has remained unclear. Although aging and androgen have been reported as definitive risk factors for BPH, recent studies have focused on the involvement of androgen-independent factors. Androgen-independent factors include ischemia, oxidative stress, metabolic syndrome, infection, autoimmune reactions, and inflammation, with inflammation in BPH tissues playing a central role in the BPH proliferative process. Inflammation in BPH tissues by various factors finally leads to tissue remodeling and stromal proliferation through the wound healing process of the prostate. To elucidate the proliferative mechanism of BPH, a study using whole-genome gene expression analysis in a stromal-dominant BPH rat model was performed and showed that immune response-related pathways and complement classical pathways are activated. Furthermore, expression analysis using this BPH rat model showed that the autoimmune reaction triggered complement pathway activation in the proliferative process of BPH. BPH is a multifactorial disease, and understanding the role of androgen-independent factors including immune responses contributes to elucidating the pathogenesis of BPH. Androgen-independent factors may lead to new therapeutic targets for BPH, and further development of this research is expected.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10380833 | PMC |
http://dx.doi.org/10.3390/ijms241411634 | DOI Listing |
J Proteome Res
December 2024
Department of Applied Biology, Indian Institute of Chemical Technology (IICT), Hyderabad 500 007, India.
Neuroendocrine prostate cancer (NEPC) is an aggressive androgen-independent PCa (AIPC) that tends to resist treatment. Understanding its progression and resistance could improve survival outcomes. Previous studies on PCa cells highlighted microsomal proteins' role in PCa progression, but their role in the progression of NEPC remains unclear.
View Article and Find Full Text PDFNat Rev Urol
October 2024
Department of Cell Biology, Montefiore Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, NY, USA.
Androgen signalling through the androgen receptor (AR) is essential for prostate tumorigenesis. However, androgen signalling pathways also interact with other growth factor-mediated signalling pathways to regulate the prostatic cell cycle, differentiation, apoptosis and proliferation in the initiation and progression of prostate cancer. Insulin-like growth factor 1 (IGF1) is one of the most prominent growth factors in prostate tumorigenesis.
View Article and Find Full Text PDFDiscov Oncol
October 2024
Department of Kidney Disease and Blood Purification, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Cancer Sci
December 2024
Department of Urology, Keio University School of Medicine, Tokyo, Japan.
Prostate cancer is initially androgen-dependent but often relapses to an androgen-independent state called castration-resistant prostate cancer (CRPC). Currently approved therapies have limited efficacy against CRPC, highlighting the need for novel therapeutic strategies. To address this need, we conducted a drug screen in our previously established aggressive CRPC cell model.
View Article and Find Full Text PDFCancer Cell
October 2024
Institute of Oncology Research (IOR), 6500 Bellinzona, Switzerland; Università della Svizzera Italiana, Faculty of Biomedical Sciences, CH6900 Lugano, Switzerland; Medical Oncology Unit, Oncology Institute of Southern Switzerland, Ente Ospedaliero Cantonale, CH6500 Bellinzona, Switzerland; Veneto Institute of Molecular Medicine, 35129 Padova, Italy; Department of Medicine, University of Padova, 35121 Padova, Italy; Department of Health Sciences and Technology (D-HEST) ETH Zurich, 8092 Zurich, Switzerland. Electronic address:
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!