Metastasis, the deadliest and most notorious feature of the disease, gives cancer the ability to spread throughout the body, often overwhelming immune defenses and even the best treatments.
Although it is a leading cause of cancer death, we still don’t know a lot about metastasis. But now researchers at the University of Cambridge’s Cancer Research UK (CRUK) Cambridge Institute have discovered a mechanism behind metastasis.
“Developing antimetastatic therapies has proven difficult because targets in primary tumors that lead to metastasis have proven difficult to find,” Eric Rahrmann, a postdoc in the lab of study leader Richard Gilbertson, told Freethink. .
The chameleon-like abilities of tumors and their protective microenvironment — a shield around them that promotes tumor growth and hinders the body’s ability to fight back — helped keep the mechanisms of metastasis elusive, Rahrmann says.
Metastasis gives cancer the ability to spread throughout the body, often overwhelming immune defenses and even the best treatments.
The new research, published in Natural genetics, identified a cell membrane protein called NALCN that serves as a sodium ion channel and acts as a “key regulator” of metastasis. These channels control the flow of sodium into and out of the cell.
Suppression or blockade of NALCN activity in mice with cancer “significantly increased the number of circulating tumor cells (CTCs) and metastases,” the authors wrote in their paper.
The study also overturns the common understanding of metastasis – that it’s just a cancer trick -: it turns out that healthy cells can also jump from organ to organ.
When NALCN was blocked in mice that never developed cancer, the researchers found that healthy cells were also released and circulated throughout the body.
They observed that healthy pancreatic cells migrated to the kidneys and then became healthy kidney cells, New Atlas reported.
“Our models demonstrated that even in the absence of a tumor, loss of NALCN function results in increased clearance of apparently normal epithelial stem cells from the bloodstream,” says Rahrmann.
Researchers have discovered a mechanism of metastasis, which we may be able to exploit to repair damaged organs in the future.
“These discoveries are among the most significant out of my lab in three decades,” Gilbertson said.
“Not only have we identified one of the elusive drivers of metastasis, but we have also overturned a common understanding of it, showing how cancer hijacks processes in healthy cells for its own gains.”
If confirmed by further research, the finding could provide a target for stopping or slowing metastasis – as well as opening the door to harnessing our own cells to repair damaged organs.
“Further investigation of this process may lead to a better understanding of how to harness our internal epithelial stem cell pools that reside in many of our organs to be mobilized throughout the body to repair us,” says Rahrmann.
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This article originally appeared on our sister site, Freethink.