Early in the 1977 movie “Star Wars,” the story’s heroes flee from the evil Empire’s minions. Accosted by a group of imperial storm troopers, Jedi Knight Obi-Wan Kenobi uses the Force to fool the soldiers into overlooking his small band of fugitive rebels.

Unfortunately, many cancers seem to have found their own version of this trick. But like Jedi knights gone rogue, they use it to a much darker purpose — they fool the body into letting tumor cells grow and spread.

Scientists Jiehui Deng, left, and Hua Yu. (Photo by Walter Urie)

City of Hope researchers found that some cancers hijack certain blood-forming cells, called myeloid cells, for their own purposes. These cells travel to other parts of the body and dupe normal tissues into creating a welcoming environment for wandering tumor cells looking for a new home.

Knowing this could help scientists find completely new approaches to keeping cancers from spreading.

When cancer cells spread, or metastasize, to other parts of the body, they may find it difficult to establish colonies in healthy tissues. Healthy tissues aren’t terribly friendly to invading cancer cells. So cancer cells recruit myeloid cells to cajole the healthy tissue into accepting the invaders.

The myeloid cells send out friendly signals to convince the normal cells in the new location to welcome the cancer, so it can take root and grow.

Researchers led by Hua Yu, Ph.D., associate chair in the Department of Cancer Immunotherapeutics and Tumor Immunology, and Jiehui Deng, Ph.D., postdoctoral fellow in Yu’s lab, found out how myeloid cells do their cancer-friendly work.

It all comes down to two important proteins: STAT3 and S1PR1.

STAT3 is highly activated in cancer cells. It boosts cancer cell growth and shields tumor cells from the body’s immune defenses.

S1PR1 can bump up STAT3’s activity. And the City of Hope scientists found that S1PR1 is highly active in myeloid cells.

So when cancer is present anywhere in the body, S1PR1, working through myeloid cells, helps boost STAT3 in normal tissues. And having more active STAT3 means a welcoming environment for roaming cancer cells looking for a new place to colonize.

“The exciting thing about our results is that they point to a whole new way we might be able to fight cancer,” Yu said. By targeting S1PR1 or the combination of S1PR1 and STAT3, researchers could keep cancer from spreading. And that could help doctors treat the cancer and completely eliminate it where it began.

The study was supported by the Tim Nesvig Lymphoma Fellowship and Research Fund, the Markel/Friedman Peritoneal Ovarian Cancer Research Fund, the W. M. Keck Foundation and the National Cancer Institute. The National Natural Science Foundation Grants of China and Abcam also supported the work.

NCI grants: CA115815, CA122976, CA115674, CA33572 and CA001727.