Scientists Decode "Molecular Chatter" That Makes Cancer Cells Spread
Principal investigator Russell Taichman, a professor at the University of Michigan (U-M) School of Dentistry in Ann Arbor, and colleagues, write about their discovery in the 30 April online issue of Nature Communications.
It is becoming increasingly clear that cancer cells are wily, well-travelled adversaries that are capable of side-stepping the treatments we throw at them to try and stop them spreading.
For instance, a recent study that produced a catalogue of the physical properties of cancer cells, found they are nimbler and more aggressive than healthy cells because they are better able to pass through small spaces, and they exert a greater force on their environment.
Now Taichman and colleagues have discovered a set of molecular signals that causes them to go into overdrive and spread.
For some time, scientists have known that tumors summon the body's healing cells, and this is a major reason cancer is difficult to treat.
Think of a cancerous tumor as a wound that won't heal: just like a benign tumor it sends out distress signals that recruit healing-type cells called mesenchymal stem cells or MSCs.
As stem cells, MSCs have the potential to differentiate into several types of cell, depending, for instance, on receiving particular conversion signals.
What Taichman and colleagues discovered is when MSCs and cancer cells interact, the molecular messages that pass between them appear to send the cancer cells into overdrive and ramp up their ability to metastasize.
"Think of giving a bunch of kids sugar, and they all go nuts," says Taichman in a statement.
He and his colleagues believe theirs is the first known study to explain the molecular behavior behind the series of changes that happen in the healing cells that result in cancer spread.
Now that we know what these messages are, we can take steps to block them, says Taichman.
For instance, it may be possible to develop drugs that can intervene earlier in the process that leads to cancer spread.
For their study, Taichman and colleagues looked at the molecular interactions between prostate and breast cancer cells and MSCs.
The interaction they decoded, starts with a signal called CXCR6, which triggers the conversion of MSCs into fibroblasts, setting off a cascade that boosts metastasis:
"CXCR6 signalling stimulates the conversion of mesenchymal stem cells into cancer-associated fibroblasts, which secrete stromal-derived factor-1, also known as CXCL12. CXCL12 expressed by cancer-associated fibroblasts then binds to CXCR4 on tumour cells and induces an epithelial-to- mesenchymal transition, which ultimately promotes metastasis to secondary tumour sites," they write.
This unique result was made possible because half of the researchers that worked on the study are experts in tumor development, and the other half are experts on wound healing.
It came about because research associate Younghun Jung, who works in Taichman's lab and is first author of the paper, works in both fields.
"It was her idea to put these together," says Taichman. "She sorted it all out, came up with the idea and finally came to me."
The study is a good example of how surprising and useful discoveries in research can result from multidisciplinary work.
Recommended related news
"Recruitment of mesenchymal stem cells into prostate tumours promotes metastasis"; Younghun Jung, Jin Koo Kim, Yusuke
Shiozawa, Jingcheng Wang, Anjali Mishra, and others; Nature Communications 4, Article number 1795, published online 30 April 2013;
DOI:10.1038/ncomms2766; Link to
Additional source: University of Michigan News Service.
Please use one of the following formats to cite this article in your essay, paper or report:
Paddock, Catharine. "Scientists Decode "Molecular Chatter" That Makes Cancer Cells Spread." Medical News Today. MediLexicon, Intl., 2 May. 2013. Web.
25 Jun. 2017. <http://www.medicalnewstoday.com/articles/259930.php>
Paddock, C. (2013, May 2). "Scientists Decode "Molecular Chatter" That Makes Cancer Cells Spread." Medical News Today. Retrieved from
Please note: If no author information is provided, the source is cited instead.