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Updated: Jul 9, 2026
A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Study of benign prostatic hyperplasia and androgen pathway manipulation on lung cancer survivals
Po-Hsin Lee1, Pang-Ting Cheng2, Ayse Celik2
1Department of Chest Medicine, Taichung Veterans General Hospital, No.1650, Sect. 4, Taiwan Boulevard, Taichung 407, Taiwan; School of Medicine, National Yang Ming Chiao Tung University, No.155, Sect. 2, Linong St., Taipei 112, Taiwan; Doctoral Program in Translational Medicine, National Chung Hsing University, No.145, Xingda Road, Taichung 402, Taiwan; Rong Hsing Translational Medicine Research Center, National Chung Hsing University, No.145, Xingda Road, Taichung 402, Taiwan.
Introduction:
Androgens and androgen receptor (AR) signaling may play a role in lung cancer pathophysiology. Patients with benign prostatic hyperplasia (BPH) may represent a population with relatively lower androgen levels, and AR signaling can be inhibited through androgen pathway manipulation (APM).
Objectives:
This study aimed to evaluate the impact of BPH and APM on survival outcomes in lung cancer patients.
Methods:
A total of 4,742 male lung cancer patients diagnosed between 2006 and 2021 were retrospectively analyzed. APM exposure referred to treatment with antiandrogens, 5-alpha reductase inhibitors, or gonadotropin-releasing hormone modulators for 30 days or longer post lung cancer diagnosis. Experimental validation was carried out using cultured A549 cells and a xenograft model in BALB/c nude mice.
Results:
Among the enrolled patients, 1,219 (25.7%) had BPH, and 121 (2.6%) were exposed to APM. Multivariable Cox analysis showed that both BPH (aHR 0.72) and APM exposure (aHR 0.63) were independently associated with improved overall survival (both p < 0.001). The in vitro study demonstrated that AR was involved in A549 cell proliferation, and that AR inhibition with finasteride decreased AR protein levels and markedly inhibited A549 cell growth. Mechanistically, finasteride promoted AR protein ubiquitination and degradation, thereby destabilizing AR protein, further inhibiting cell cycle progression, and inducing apoptosis in A549 cells. In addition, the in vivo results corroborated finasteride's inhibitory effect on lung cancer growth.
Conclusions:
These findings suggest that both BPH and APM exposure were associated with improved survival in male patients with lung cancer. Finasteride disruption of AR stability might subsequently inhibit A549 lung cancer cell growth. Overall, these results highlight the potential therapeutic value of targeting androgen and AR signaling in lung cancer treatment.