Bone Marrow Adipocyte: An Intimate Partner With Tumor Cells in Bone Metastasis

被引:45
|
作者
Luo, Guojing [1 ]
He, Yuedong [2 ]
Yu, Xijie [1 ]
机构
[1] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Dept Endocrinol & Metab,Lab Endocrinol & Metab, Chengdu, Sichuan, Peoples R China
[2] Sichuan Univ, West China Univ Hosp 2, Dept Gynecol, Chengdu, Sichuan, Peoples R China
来源
FRONTIERS IN ENDOCRINOLOGY | 2018年 / 9卷
基金
中国国家自然科学基金;
关键词
bone marrow adipocyte; adipose; bone metastasis; interleukin-6; tumor necrosis factor-alpha; leptin; adiponectin; EPITHELIAL-MESENCHYMAL TRANSITION; TO-ADIPONECTIN RATIO; FATTY-ACID OXIDATION; ADIPOSE-TISSUE; PROSTATE-CANCER; BREAST-CANCER; LUNG-CANCER; LEPTIN-RECEPTOR; PARATHYROID-HORMONE; MULTIPLE-MYELOMA;
D O I
10.3389/fendo.2018.00339
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The high incidences of bone metastasis in patients with breast cancer, prostate cancer and lung cancer still remains a puzzling issue. The "seeds and soil" hypothesis suggested that bone marrow (soil) may provide a favorable "niche" for tumor cells (seed). When seeking for effective ways to prevent and treat tumor bone metastasis, most researchers focus on tumor cells (seed) but not the bone marrow microenvironment (soil). In reality, only a fraction of circulating tumor cells (CTCs) could survive and colonize in bone. Thus, the bone marrow microenvironment could ultimately determine the fate of tumor cells that have migrated to bone. Bone marrow adipocytes (BMAs) are abundant in the bone marrow microenvironment. Mounting evidence suggests that BMAs may play a dominant role in bone metastasis. BMAs could directly provide energy for tumor cells, enhance the tumor cell proliferation, and resistance to chemotherapy and radiotherapy. BMAs are also known for releasing some inflammatory factors and adipocytokines to promote or inhibit bone metastasis. In this review, we made a comprehensive summary for the interaction between BMAs and bone metastasis. More importantly, we discussed the potentially promising methods for the prevention and treatment of bone metastasis. Genetic disruption and pharmaceutical inhibition may be effective in inhibiting the formation and pro-tumor functions of BMAs.
引用
收藏
页数:14
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