Inhibition of a corrupted embryonic developmental regulator reverses colon cancer to a normal-like state [TAF10 ChIP-seq]

A systems approach could identify mechanisms to drive the reversion of cancer cells into normal-like cells. Here, we identify the transition state between normal and cancer cells in colon and show that knockdown of TATA-box-binding-protein-associated Factor 10 (TAF10) can rewire the gene regulatory network, resulting in reversion of colon cancer cells into normal-like cells.

Intriguingly, TAF10 is essential in embryonic development and should be inactivated after development, but is instead hijacked during colon cancer tumorigenesis and remains as a potential reversion switch of the underlying complex molecular network.