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PETBioNewsNewsGenome editing used to slow cancer growth

BioNews

Genome editing used to slow cancer growth

Published 13 June 2017 posted in News and appears in BioNews 902

Author

Annabel Slater

Image by Peter Artymiuk via the Wellcome Collection. Depicts the shadow of a DNA double helix, on a background that shows the fluorescent banding of the output from a DNA sequencing machine.
CC BY 4.0
Image by Peter Artymiuk via the Wellcome Collection. Depicts the shadow of a DNA double helix, on a background that shows the fluorescent banding of the sequencing output from an automated DNA sequencing machine.

US scientists have delayed cancer cell growth by using genome editing to remove a protein...

US scientists have delayed cancer cell growth by using genome editing to remove a protein.

Removing an enzyme known as Tudor-SN delayed the replication of cells from human kidney and cervical cancers in the lab.

'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 Dr Reyad Elbarbary of the University of Rochester, New York, and lead author.

Normal cells divide and replicate through the process known as the cell cycle. If the cycle is disrupted, cells can become cancerous and replicate uncontrollably, forming tumours.

One regulatory component of the cell cycle is micro RNA (miRNA) - small noncoding RNA molecules which adjust gene expression. The Rochester team showed that removing Tudor-SN through genome editing increased the amount of miRNA present. The miRNA reduced the expression of genes critical to the progression of the cell cycle from the 'preparatory' phase to the replication phase.

Although the research is at a very early stage, the team hope their findings could lead to a new treatment option for cancer. They next plan to investigate how Tudor-SN works with other molecules in the cell cycle, in order to develop drugs to target it.

'Because cancer cells have a faulty cell cycle, pursuing factors involved in the cell cycle is a promising avenue for cancer treatment,' said Professor Lynne Maquat of the University of Rochester, and senior author.

Dr Thomas Cox of the Garvan Institute of Medical Research, Australia, who was not involved in the study, told Cosmos magazine that targeting miRNA is difficult and technically challenging. 'This study is saying: "Well, if we can’t target microRNAs directly, can we target something regulating them?"'

The study was published in Science.

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