Qianliening capsule treats benign prostatic hyperplasia (BPH) via suppression of epidermal growth factor/signal transducer and activator of transcription 3 (EGF/STAT3) signaling pathway

2012 ◽  
Vol 6 (12) ◽  
Author(s):  
Jiumao Lin
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Prostatic Hyperplasia ◽  
Signal Transducer ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Epidermal Growth ◽  
Transcription 3 ◽  
Epidermal Growth Factor Signal

scholarly journals Interplay of Epidermal Growth Factor Receptor and Signal Transducer and Activator of Transcription 3 in Prostate Cancer: Beyond Androgen Receptor Transactivation

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3452
Author(s):  
Shian-Ren Lin ◽  
Hsiu-Lien Yeh ◽  
Yen-Nien Liu
Keyword(s):  
Prostate Cancer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Signal Transducer ◽  
Stat3 Signaling ◽  
Castration Resistant ◽  
Epidermal Growth ◽  
Transcription 3 ◽  
Further Development

Prostate cancer (PCa) is one of the most common cancers in the world and causes thousands of deaths every year. Conventional therapy for PCa includes surgery and androgen deprivation therapy (ADT). However, about 10–20% of all PCa cases relapse; there is also the further development of castration resistant adenocarcinoma (CRPC-Adeno) or neuroendocrine (NE) PCa (CRPC-NE). Due to their androgen-insensitive properties, both CRPC-Adeno and CRPC-NE have limited therapeutic options. Accordingly, this study reveals the inductive mechanisms of CRPC (for both CRPC-Adeno and CRPC-NE) and fulfils an urgent need for the treatment of PCa patients. Although previous studies have illustrated the emerging roles of epidermal growth factor receptors (EGFR), signal transducer, and activator of transcription 3 (STAT3) signaling in the development of CRPC, the regulatory mechanisms of this interaction between EGFR and STAT3 is still unclear. Our recent studies have shown that crosstalk between EGFR and STAT3 is critical for NE differentiation of PCa. In this review, we have collected recent findings with regard to the involvement of EGFR and STAT3 in malignancy progression and discussed their interactions during the development of therapeutic resistance for PCa.

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