Melatonin interrupts osteoclast functioning and suppresses tumor-secreted RANKL expression: implications for bone metastases

doi:10.1038/s41388-020-01613-4

中山醫學大學機構典藏 CSMUIR > 中山醫學大學研究成果 > 期刊論文 > Item 310902500/23655

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/23655

Title:	Melatonin interrupts osteoclast functioning and suppresses tumor-secreted RANKL expression: implications for bone metastases
Authors:	Liu, PI;Chang, AC;Lai, JL;Lin, TH;Tsai, CH;Chen, PC;Jiang, YJ;Lin, LW;Huang, WC;Yang, SF;Tang, CH
Date:	2021
Issue Date:	2022-08-05T09:40:46Z (UTC)
Publisher:	SPRINGERNATURE
ISSN:	0950-9232
Abstract:	Cancer-related bone erosion occurs frequently in bone metastasis and is associated with severe complications such as chronic bone pain, fractures, and lower survival rates. In recognition of the fact that the darkness hormone melatonin is capable of regulating bone homeostasis, we explored its therapeutic potential in bone metastasis. We found that melatonin directly reduces osteoclast differentiation, bone resorption activity and promotes apoptosis of mature osteoclasts. We also observed that melatonin inhibits RANKL production in lung and prostate cancer cells by downregulating the p38 MAPK pathway, which in turn prevents cancer-associated osteoclast differentiation. In lung and prostate bone metastasis models, twice-weekly melatonin treatment markedly reduced tumor volumes and numbers of osteolytic lesions. Melatonin also substantially lowered the numbers of TRAP-positive osteoclasts in tibia bone marrow and RANKL expression in tumor tissue. These findings show promise for melatonin in the treatment of bone metastases.
URI:	http://dx.doi.org/10.1038/s41388-020-01613-4 https://www.webofscience.com/wos/woscc/full-record/WOS:000607998600005 https://ir.csmu.edu.tw:8080/handle/310902500/23655
Relation:	ONCOGENE ,2021,v40,issue 8, P1503-1515
Appears in Collections:	[中山醫學大學研究成果] 期刊論文

Files in This Item:

File	Description	Size	Format
index.html		0Kb	HTML	212	View/Open

Loading...