Rongé. normal bone ( left ) is a solid mass. But relaxin stimulates the body's own cells to eat holes in the (white dot).
A similar hormone insulin accelerates the destruction of the bone caused by malignant tumors, a team of clinical pathologists found. "The study addresses a fundamental question," says Jonathan Waxman, an oncologist at Imperial College London. If confirmed, the findings could eventually point to drugs to slow or stop the bone damage caused by cancers.
Known as relaxin, the hormone had already been linked to cancer. previous studies have linked high levels of relaxin for endometrial cancer and aggressive prostate and cancers that spread bone, like the breast, thyroid, and myeloma. But if relaxin produced by cancerous tumors could stimulate bone destruction remained unclear.
indirect evidence suggested that it might said Alberto Ferlin and Carlo Foresta, clinical pathologists at the University of Padua in Italy and co-author of the new study. Relaxin belongs to the same class of hormones that produced in the testes called INSL3. In previous work with the mouse and human cells in culture, Ferlin and his colleagues have shown that, under certain conditions, INSL3 interacts with cells called osteoblasts that build bone. When the testes do not produce enough INSL3, bone mass decreases and osteoporosis occurs. "We thought that relaxin could trigger a similar effect," said Ferlin. "We were right."
The researchers demonstrated that by studying the effects of relaxin on cells in human bone culture. They found that the hormone stimulates osteoclast cells, which normally combine osteoblast activity by removing excess bone through a mechanism called resorption. By binding to a receptor molecule called RXFP1 on the surface of osteoclasts, resorption relaxin triggered runaway, causing osteoclasts to consume too much bone and release a large amount of calcium. In the body, such a calcium influx into the blood causes hypercalcemia, severe impairment usually associated with the presence of bone metastases. The researchers also found that relaxin promotes growth, differentiation and invasiveness of various tumors, particularly those that give bone metastases.
When the researchers added an anti-relaxin antibodies in cell cultures, the antibody prevents relaxin to bind with receptors and trigger bone lesions. This finding, they fall in the number 2 February Os , suggests that a drug based on this antibody or which inhibits the receptor relaxin may slow bone lesions while preventing hypercalcemia, said Foresta .
"It seems almost too good to be true," said Waxman, who said the results could be "the point of embarking on a journey" toward treatments that stop the spread of bone cancer. Find such a drug will not necessarily be a short trip, however. Regarding the targeting of RXFP1 receiver, Ferlin and Foresta say there peptides already available for this purpose. However, they also point out that a new drug designed to target the receptor would be completely new, so side effects are unknown.
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