학술논문

Prostate cancer and bone: clinical presentation and molecular mechanisms.
Document Type
article
Source
Endocrine Related Cancer. 30(9)
Subject
Prostate Cancer
Aging
Cancer
Urologic Diseases
Musculoskeletal
Male
Humans
Prostatic Neoplasms
Bone Neoplasms
Androgen Antagonists
Bone and Bones
Treatment Outcome
Tumor Microenvironment
androgen receptor
bone
hypoxia
metastasis
prostate cancer
tissue engineering
Biological Sciences
Medical and Health Sciences
Oncology & Carcinogenesis
Language
Abstract
Prostate cancer (PCa) is an increasingly prevalent health problem in the developed world. Effective treatment options exist for localized PCa, but metastatic PCa has fewer treatment options and shorter patient survival. PCa and bone health are strongly entwined, as PCa commonly metastasizes to the skeleton. Since androgen receptor signaling drives PCa growth, androgen-deprivation therapy whose sequelae reduce bone strength constitutes the foundation of advanced PCa treatment. The homeostatic process of bone remodeling - produced by concerted actions of bone-building osteoblasts, bone-resorbing osteoclasts, and regulatory osteocytes - may also be subverted by PCa to promote metastatic growth. Mechanisms driving skeletal development and homeostasis, such as regional hypoxia or matrix-embedded growth factors, may be subjugated by bone metastatic PCa. In this way, the biology that sustains bone is integrated into adaptive mechanisms for the growth and survival of PCa in bone. Skeletally metastatic PCa is difficult to investigate due to the entwined nature of bone biology and cancer biology. Herein, we survey PCa from origin, presentation, and clinical treatment to bone composition and structure and molecular mediators of PCa metastasis to bone. Our intent is to quickly yet effectively reduce barriers to team science across multiple disciplines that focuses on PCa and metastatic bone disease. We also introduce concepts of tissue engineering as a novel perspective to model, capture, and study complex cancer-microenvironment interactions.