This trick boosts cancer’s spread

From Washington, D.C., at the Experimental Biology 2007 Conference

A molecule on the surface of most cells keeps them tightly stitched together into well-organized tissues. Because such order prevents the cells from growing excessively or leaving the tissue, spreading cancer cells turn off the production of this molecule, called E-cadherin. A new study shows that, contrary to conventional medical wisdom, that shutdown isn’t permanent.

And that could be bad news.

The loss of E-cadherin makes a cancer cell resemble a stem cell in its capacity to assume any tissue type, notes University of Pittsburgh pathologist Alan Wells. It also makes those cells look different from those in normal tissues.

However, once a spreading, or metastatic, cell lands in a hospitable new tissue, it can reboot E-cadherin production and take on the appearance of a well-behaved neighbor, Wells and his coworkers have found. In fact, the spreading cells are anything but model neighbors.

Triggered by as-yet-unrecognized signals, the cancer cells can resume unchecked growth in their new homes and then spread farther, notes Wells’ Pittsburgh colleague, Christopher R. Shepard.

The team experimented with breast cancer cells excised from 11 women. All the cells were initially free of E-cadherin, but within 6 days of being incubated with healthy liver cells, the cancer cells from three women resumed E-cadherin production.

In the April 23 British Journal of Cancer, the Pittsburgh team reports similar behavior in prostate cancer cells following their incubation with liver cells.

Wells says that although the re-emergence of E-cadherin makes cancer cells look “almost benign,” that’s just a “disguise.” It might even protect cancer cells against elimination by chemotherapy agents that target rapidly proliferating cells.