Open AccessMolecular Regulation of Bone Metastasis Pathogenesis
Author(s) -
MengYu Wu,
ChiaJung Li,
GiouTeng Yiang,
Yeung-Leung Cheng,
Andy P. Tsai,
Yueh-Tseng Hou,
Yu-Chieh Ho,
MingFeng Hou,
PeiYi Chu
Publication year - 2018
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000489184
Subject(s) - rankl , osteoprotegerin , cancer research , medicine , bone metastasis , bone marrow , tumor microenvironment , bone remodeling , metastasis , immune system , cancer , myeloid derived suppressor cell , immunology , receptor , activator (genetics) , suppressor
Distant metastases are the major cause of mortality in cancer patients. Bone metastases may cause bone fractures, local pain, hypercalcemia, bone marrow aplasia, and spinal cord compression. Therefore, the management of bone metastases is important in cancer treatment. Normal bone remodeling is regulated by osteoprotegerin ligand (OPGL), receptor activator of NF-κB ligand (RANKL), parathyroid hormone-related protein (PTHrP), and other cytokines. In the tumor microenvironment, tumor cells induce a vicious cycle that promotes osteoblastic and osteolytic lesions. Studies support the idea that distant metastases may occur due to the immunosuppressive function of myeloid-derived suppressor cells (MDSCs). These cells inhibit T cells and natural killer (NK) cells and differentiate into tumor-associating macrophages (TAMs), monocytes, and dendritic cells (DCs). In this review, we summarize studies focusing on the role of MDSCs in bone metastasis and provide a strong foundation for developing anticancer immune treatments and anticancer therapies, in general.