Osteoblasts and osteoclasts: an important switch of tumour cell dormancy during bone metastasis

Table 3 Self-control of dormant tumour cells by utilizing bone remodelling

Self-control	Dormant cancer types	Reactions	Mechanisms	Reference
Reactivate from dormancy	Breast cancer cells	↑ VCAM-1	↑ the recruitment of osteoclast precursors; directly interacting with the cognate receptor integrin α4β1; ↑ preosteoclasts’ adhesion to dormant breast tumour cells	[24]
Reactivate from dormancy	Breast cancer cells and giant cell tumour of bone	↑ PTHrP	↓ pro-dormancy gene expression; ↑ osteoclastogenesis and bone resorption through ↑ RANKL expression in an autocrine manner	[29, 53]
Maintain dormancy	Breast cancer cells	↑ N-Cadherin	↑ the adhesive attraction of MDA to SNOs	[54]
	Prostate cancer cells	↑ ROR2	↑ Wnt5a-induced dormancy driven by osteoblasts	[28]
	Prostate cancer cells	↑ Axl	Gas6/Axl signalling ↑ expression of TGFβ2 and its receptor	[55, 56]
	Prostate cancer cells	↑ TBK1	After binding to osteoblasts,↓ mTOR and ↑ drug resistance to chemotherapy	[57]
	Acute lymphoblastic leukemia cells	Express OPN receptors	Compete with HSCs for adhesion to OPN within the bone marrow	[23]
	Acute lymphoblastic leukemia cells	Express CXCR4	Compete with HSCs for binding to CXCL12 in the bone marrow	[58, 59]
	Prostate cancer cells and myeloma cells	Express Annexin II receptor	Compete with HSCs for binding to annexin II on osteoblasts	[32, 60, 61]
	Prostate cancer cells	N/A	↑ haematopoietic differentiation, replace and mobilize HSCs from the osteoblastic niche	[6]

Note: ‘↑’ represents increased, upregulated, induced, accelerated, enhanced and activated; While ‘↓’ represents decreased, downregulated, inhibited; N/A represents not applicable

ISSN: 1756-9966