Signals can direct cells to act cancerous, surviving, growing and replicating uncontrollably.
And signals can also tell cells with cancerous characteristics to stop growing or to die. In breast cancer, one tricky signal called TGF-beta does both - sometimes promoting tumours and sometimes suppressing them.
A University of Colorado Cancer Center study details how tumours may flip the TGF-beta signalling switch, allowing doctors to delete the pathway entirely when it promotes tumours, and leave it intact when it's still working to suppress them.
Embryos grow quickly and so require cells that proliferate quickly and are able to move to other areas of the embryo.
Early in human development, we depend on a transcription factor called SIX1 to create this weed-like growth and nimble movement. Then, as adults, we turn off this SIX1 pathway in most cells - we no longer need explosive growth or movement and so the pathway goes to sleep in our genome.
Many breast cancers wake SIX1, and the Oncogene paper details how SIX1 flips the TGF-beta signalling switch from tumor-suppressing or tumor-promoting.
SIX1 creates small molecules called microRNAs that regulate gene activity. In this case, SIX1's microRNAs attach to and mute the section of TGF-beta that stops cell growth. With TGF-beta silenced, the signal does nothing to stop cell growth, and instead encourages these cells to migrate into new tissues.
Turning on SIX1 and its associated microRNAs is like removing the speed governor from a reckless teenager's Mustang convertible.
"High SIX1 or high microRNAs associated with SIX1 are a sign that a breast cancer is using TGF-beta signaling in a tumor-promoting way," Ford said.
Patients whose tumours have high SIX1 or associated microRNAs are likely to benefit from "TGF-beta inhibitors" - drugs that turn off the signal - that are currently in clinical trials.
Conversely, patients with low SIX1 are best left with TGF-beta signalling intact - in this case, the signal is likely helping these breast cancer patients fight against their tumours.
In the future, Ford hopes to target SIX1 directly.
"Because we don't need it in most adult tissues, if we could target SIX1, we could probably inhibit the tumor on multiple fronts with few side effects," she added.
The study has been published in the journal Oncogene.