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Interactions between breast cancer, osteoblastic cells induce osteoclastogenesis.

Women's Health Weekly

| November 06, 2003 | COPYRIGHT 2003 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2003 NOV 6 - (NewsRx.com & NewsRx.net) -- Direct interactions between breast cancer and stromal or osteoblastic cells induce osteoclastogenesis through modulating RANKL expression.

"Bone destruction is primarily mediated by osteoclastic bone resorption, and cancer cells stimulate the formation and activation of osteoclasts next to metastatic foci," scientists in South Korea report.

"Accumulating evidences indicate that receptor activator of NFkappaB ligand (RANKL) is the ultimate extracellular mediator that stimulates osteoclast differentiation into mature osteoclasts. In contrast, osteoprotegerin (OPG) inhibits osteoclast development," wrote H.R. Park and colleagues, Hallym University, Sacred Heart Hospital.

"In order to elucidate a mechanism for cancer-induced osteoclastogenesis, cells from a human breast cancer line, MDA-MB-231, were directly co-cultured with ST2, MC3T3-E1, or with primary mouse calvarial cells. Osteoclast-like cells and tartarate resistant acid phosphatase (TRAP) activities were then quantitated," the researchers wrote.

"We examined these cell lines and samples from breast cancer by RT-PCR for the expressions of OPG and RANKL mRNA. Compared to controls, co-culture of MDA-MB-231 cells with stromal or osteoblastic cells induced an ...

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