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Latrophilin-3 as a downstream effector of the androgen receptor induces bladder cancer progression
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Latrophilin-3 as a downstream effector of the androgen receptor induces bladder cancer progression
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Journal Article
Latrophilin-3 as a downstream effector of the androgen receptor induces bladder cancer progression
2024
Overview
Emerging evidence indicates that androgen receptor (AR) signaling plays a critical role in the pathogenesis of male-dominant urothelial cancer and its outgrowth. Meanwhile, latrophilins (LPHNs), a group of the G-protein-coupled receptors to which a spider venom latrotoxin (LTX) is known to bind, remain largely uncharacterized in neoplastic diseases. The present study aimed to determine the functional role of LPHN3 (encoded by the
ADGRL3
gene), in association with AR signaling, in the progression of bladder cancer. In AR-positive bladder cancer lines, dihydrotestosterone considerably increased the expression levels of
ADGRL3
and LPHN3, while chromatin immunoprecipitation assay revealed the binding of AR to the promoter region of
ADGRL3
. Treatment with LPHN3 ligands (e.g. α-LTX, FLRT3) resulted in the induction of
ADGRL3
expression, as well as cell viability, in bladder cancer lines. By contrast, LPHN3 knockdown via shRNA virus infection significantly reduced the viability and migration of these cells. Immunohistochemistry in transurethral resection specimens further showed a strong correlation between LPHN3 and AR expression. Moreover, LPHN3 positivity in muscle-invasive bladder tumors, as an independent prognosticator, was associated with a significantly higher risk of disease progression and disease-specific mortality following radical cystectomy. These findings suggest that LPHN3 functions as a downstream effector of AR and promotes the growth of bladder cancer.
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