Using CRISPR gene editing to slow cancer growth

Cancer
CRISPR gene editing may help slow the rapid cell division that's characteristic of all cancers.

The gene editing technology CRISPR/CAS9 is being used to develop a host of new treatments, mostly for genetic diseases. But researchers from the University of Rochester's Center for RNA Biology are investigating whether gene editing can be used for another purpose: to slow the growth of cancer cells.

Although there are many types of cancer, they’re all characterized by the same uncontrollable cell growth. So the University of Rochester team is targeting the cell cycle, which is the series of events that leads to cell growth and division, according to a press release. And they’ve zeroed in on a single protein, called Tudor-SN, that’s a key element in the preparatory phase of cell division.

Using CRISPR, the scientists eliminated Tudor-SN from cells. Then they observed that those cells were taking much longer to prepare for division.

"We know that Tudor-SN is more abundant in cancer cells than healthy cells, and our study suggests that targeting this protein could inhibit fast-growing cancer cells," said Reyad A. Elbarbary, Ph.D., a research assistant at the University of Rochester and the lead author, in the release.

Elbarbary works in a lab that discovered that Tudor-SN influences the cell cycle by controlling microRNAs, according to the release. When the protein is removed, levels of many types of microRNAs rise, which in turn switches off genes that promote cell growth.

This isn’t the first time CRISPR has been proposed in the context of finding new ways to attack cancer. Last year, Facebook and Napster billionaire Sean Parker turned heads when his Parker Institute funded research at the University of Pennsylvania that’s focused on editing T cells—immune cells that usually can’t recognize cancer as a foreign invader. The Penn scientists are using CRISPR to edit out genes of T cells in the hopes of enabling the immune system to search out and kill cancer cells.

Eliminating Tudor-SN through gene editing is more about disrupting the very process that results in cancer—abnormal cell proliferation. There are already molecules in the clinic that target Tudor-SN, Elbarbary says, making it possible to consider cancer therapies based on this mechanism. The University of Rochester team plans further studies to determine how Tudor-SN works with other proteins so they can best identify drugs that will target cell division.