Blocking the action of an enzyme called GnT-V could delay the onset and spread of tumours with human breast cancer, a new study has found.
When the GnT-V enzyme activity in the cells was increased in mammary gland cells, they increased proliferation and began to take on many characteristics of cancer cells.
Using a mouse model of human breast cancer, tumours appeared when the enzyme was deleted, but onset was delayed an average of 10 weeks in the mice.
"In human terms, the corresponding delay would be many months and maybe years. You basically are slowing everything down and keeping the cancer from forming and progressing very early," said Michael Pierce, study co-author.
Slowing the pace of the cancer could eliminate its spread to other organs, keeping it localized where it could be treated successfully, explained Pierce.
The researchers, lead by Hua-Bei Guo, stimulated breast cancer formation in mouse mammary glands by over-expressing a her-2 protein that is a growth receptor on the cell surface.
The GnT-V enzyme makes glycans, which are sugars on the cell surface that change in defined ways when the cell becomes cancerous. Glycans are released from the cell as glycoproteins, making them a promising early-detection marker in blood.
The researchers studied a glycan made by GnT-V that appears when normal breast cells become cancerous. The GnT-V glycan product is found on her-2 and other receptors and acts to regulate the number of cancer stem cells in the tissue.
"This study is an example of how particular glycans that are present on various cell receptors can actually modulate the onset of tumour formation. That may give us new drug targets and new ways to kill the cancer cells specifically," said Pierce.
The research was published in the journal Proceedings of the National Academy of Sciences.