Loss of CTCF leads to inactivation of tumour suppressors

This article was published in Molecular Cell on May 15, 2009, titled “EVEN IN OUR GENOME, GOOD FENCES MAKE GOOD NEIGHBOURS” (http://www.sciencedaily.com/releases/2009/05/090514125146.htm).

It outlines recent findings that how our genome is structured and packed into cells may affect our chances of getting cancer. In a normal cell, there are both tumour suppressor enzymes and cell growth enzymes which keep cell growth and division at a normal rate. Scientists have found that by affecting certain parts of the genome can cause repercussions all down it, leading to changes in growth. In many types of cancer, the tumour suppressor p16 gets stuck in the middle of the condensed chromatin so it can’t be unwound and expressed as easily, leading to abnormal cell replication.

What has recently been discovered though is that the CTCF or CCCTC-binding factor which separates the tightly coiled chromatin from the rest of the genome lost several proteins and fell off, meaning the heterochromatin coiled around the p16 suppressor and silenced it. The CTCF that did not bind was missing a crucial protein called poly(ADP-ribosyl)ation. Without this protein, the CTCF doesn’t form the necessary complex and so suppressors end up being silenced in the cells.

By Ellinor Johnston