CRISPR gene editing puts the brakes on cancer cells


Removing the Tudor-SN protein from cancerous cells slows down their growth. Anthea Batsakis reports.


A cancer cell in the process of division. Knocking out the Tudor-SN protein might have stopped things getting this far.
Steve Gschmeissner / Getty

Cancer cells are known for their fast and rapacious growth, but a new technique to slow them down may one day offer new treatment options.

Scientists from the US have discovered a protein called Tudor-SN linked to the “preparatory” phase of cell life – when cells prepare to divide and spread.

Using the gene-editing technology CRISPR, the researchers removed the protein, which is more abundant in cancer cells than healthy cells, and found cancer cell growth was effectively delayed.

The research team, led by Reyad Elbarbary and Keita Myoshi from the University of Rochester, in New York, made its findings in a laboratory using cells from kidney and cervical cancers.

While the technique is still far from human trials, the researchers report in the journal Science that their findings could potentially be used as a treatment option.

Thomas Cox from the Garvan Institute of Medical Research in Sydney, who wasn’t involved in the study, says there is potential for the technique to boost the effectiveness of some standard therapies by slowing tumour cells down.

The treatment works by hacking into molecules involved in the life cycle of cancerous cells.

Healthy cells go through a cycle of growth, division and death. For cancerous cells, this cycle is faulty and the cells grow abnormally and uncontrollably, infiltrating nearby tissues.

The protein’s effect on the cell cycle is a result of its influence on microRNAs – the molecules that determine what genes are switched on and when, including the genes that control cell growth.

Plucking out Tudor-SN boosted the number of certain microRNAs that, in turn, prevented the production of proteins responsible for cell growth.

Cox says the process of targeting microRNAs is difficult and technically challenging:

“This study is saying: ‘Well, if we can’t target microRNAs directly, can we target something regulating them?’ ”

MicroRNAs have long been known to be involved in cancer, and recent studies have also looked at the influence of Tudor-SN. What this present research does differently, Cox says, is home in on how these affect the cell cycle.

The next step, he adds, will be testing the treatment in mice.

Anthea Batsakis is a freelance journalist in Melbourne, Australia.
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