1. 1,25(OH)2D3 deficiency increases TM40D tumor growth in bone and accelerates tumor-induced bone destruction in a breast cancer bone metastasis model
- Author
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Ziyi Fu, Yongmei Yin, Dengshun Miao, Jun Li, Shidai Jin, Jiahui Chu, and Guangping Lu
- Subjects
0301 basic medicine ,Pharmacology ,Oncology ,medicine.medical_specialty ,business.industry ,Bone metastasis ,General Medicine ,medicine.disease ,In vitro ,vitamin D deficiency ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Breast cancer ,In vivo ,030220 oncology & carcinogenesis ,Internal medicine ,Knockout mouse ,medicine ,Vitamin D and neurology ,Tumor growth ,skin and connective tissue diseases ,business - Abstract
Breast cancer is one of the most common malignancies and bone is the commonest site of distant metastases. Evidences indicate that adequate supply of vitamin D will decrease the morbidity and mortality of breast cancer. However, the main role of vitamin D deficiency in breast cancer bone metastases remains unclear. In this study, the relationship between vitamin D and breast cancer bone metastases were evaluated. Results showed that 1,25(OH)2D3 can not only inhibit the proliferation, migration and invasion of breast cancer cell TM40D in vitro, but also attenuate the breast cancer cell TM40D-induced bone destruction in vivo, whose underlying mechanism was at least partially through decreasing the number of the osteoclasts. To our knowledge, this is the first to use 1-alpha-hydroxylase [1α(OH)ase] knockout mice which characterized vitamin D deficiency to establish the breast cancer bone metastases model. Based on this model, we also found that vitamin D deficiency will accelerate the osteolytic lesions, and 1,25(OH)2D3 supplement will restrain osteolytic lesions. Therefore, these findings suggest that vitamin D has the potential capacity to be a therapeutic agent for the breast cancer bone metastases.
- Published
- 2017