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Decoded: Molecular messages that tell prostate and breast cancers to spread

Date:
April 30, 2013
Source:
University of Michigan
Summary:
Cancer cells are wily, well-traveled adversaries, constantly side-stepping treatments to stop their spread. But for the first time, scientists have decoded the molecular chatter that ramps certain cancer cells into overdrive and can cause tumors to metastasize throughout the body.

Tumor cells secrete signals that call in wound healing cells to the tumor site. In the process, the normal wound healing cells make the tumor cells more aggressive and able to metastasize.
Credit: Image courtesy of University of Michigan

Cancer cells are wily, well-traveled adversaries, constantly side-stepping treatments to stop their spread. But for the first time, scientists at the University of Michigan have decoded the molecular chatter that ramps certain cancer cells into overdrive and can cause tumors to metastasize throughout the body.

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Researchers have long known that tumors recruit healing cells, which is a major reason why cancer is so difficult to thwart. This is the first known study to explain the molecular behavior behind the series of changes that happen in the healing cells that result in metastasis.

Russell Taichman, a professor at the U-M School of Dentistry and research associate Younghun Jung looked at prostate and breast tumors. Their study, "Recruitment of mesenchymal stem cells into prostate tumors promotes metastasis," appears April 30 in the online journal Nature Communications.

Consider that a tumor is a wound that won't heal. To that end, both cancerous and benign tumors emit distress signals and messages to recruit healing-type cells, called mesenchymal stem cells, or MSCs, Taichman said.

"Now we know what messages (tumors) send to recruit and alter those healing cells, and we can take steps to block those messages," said Taichman, the study's principal investigator.

With this information, researchers can now try to develop drugs to pharmaceutically derail tumor formation earlier. This is especially important because this particular molecular signaling involves reactions among proteins that actually make cancer cells more migratory, more aggressive and more likely to spread.

To that end, Taichman said he was surprised at the large role played by the protein CXCL16 in altering the healing type cells in such a way that they revved the cancer cells into overdrive.

"Think of giving a bunch of kids sugar, and they all go nuts," he said.

On a personal level, the way the results emerged also delighted Taichman. Half of the researchers in Taichman's lab work on tumor development and half on wound healing. The research of Jung, the first author on the study, straddles both.

"It was her idea to put these together," Taichman said. "She sorted it all out, came up with the idea and finally came to me."


Story Source:

The above story is based on materials provided by University of Michigan. The original article was written by Laura Bailey. Note: Materials may be edited for content and length.


Journal Reference:

  1. Younghun Jung, Jin Koo Kim, Yusuke Shiozawa, Jingcheng Wang, Anjali Mishra, Jeena Joseph, Janice E. Berry, Samantha McGee, Eunsohl Lee, Hongli Sun, Jianhua Wang, Taocong Jin, Honglai Zhang, Jinlu Dai, Paul H. Krebsbach, Evan T. Keller, Kenneth J. Pienta, Russell S. Taichman. Recruitment of mesenchymal stem cells into prostate tumours promotes metastasis. Nature Communications, 2013; 4: 1795 DOI: 10.1038/ncomms2766

Cite This Page:

University of Michigan. "Decoded: Molecular messages that tell prostate and breast cancers to spread." ScienceDaily. ScienceDaily, 30 April 2013. <www.sciencedaily.com/releases/2013/04/130430131645.htm>.
University of Michigan. (2013, April 30). Decoded: Molecular messages that tell prostate and breast cancers to spread. ScienceDaily. Retrieved December 21, 2014 from www.sciencedaily.com/releases/2013/04/130430131645.htm
University of Michigan. "Decoded: Molecular messages that tell prostate and breast cancers to spread." ScienceDaily. www.sciencedaily.com/releases/2013/04/130430131645.htm (accessed December 21, 2014).

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