β-catenin is a protein that helps regulate gene transcription and binding cells to create larger structures. As such, β-catenin is important to normal embryonic development and is linked to tumor development and cancer. Therefore, targeting β-catenin as a way to treat cancer has received a lot of scientific attention, but the factors involved remain unclear.

Mao’s research team has isolated RNF220 as a regulator of β-catenin, and promotes canonical Wnt signaling. In other word, RNF220 helps β-catenin cross through the cell and into the nucleus where gene transcription happens. When this doesn’t happen, β-catenin accumulates which is involved in the development of cancer. Normally, when β-catenin isn’t used it is destroyed, but in cancer this isn’t always the case. Therefore, preventing the accumulation of β-catenin could be a viable method of treating cancer.

Mao and his team have not only identified RNF220 as an important regulator, but have also worked to clarify how it helps to inhibit β-catenin. More specifically, RNF220 interacts with USP7, a peptidase, to enhance canonical Wnt signaling. They have also discovered a positive feedback cycle whereby the components that work to destroy β-catenin also act to inhibit RNF220, and vice versa. This discovery suggests the novel role of RNF220 in cancer treatment and prevention.

The results of the study have been published in Molecular and Cellular Biology available here: http://mcb.asm.org/content/early/2014/09/23/MCB.00731-14.long

(By Andrew Willden)