New UGA research, published in the early online edition of the journal Proceedings of the National Academy of Sciences, has found that blocking the action of an enzyme called GnT-V significantly delays the onset and spread of tumors in mice with cancer very similar to many cases of human breast cancer.
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, tumors appeared when the enzyme was deleted, but onset was delayed an average of 10 weeks in the mice.
Slowing the pace of the cancer could eliminate its spread to other organs, keeping it localized where it could be treated successfully, according to Michael Pierce, director of the UGA Cancer Center and study co-author.
The researchers, lead by Hua-Bei Guo, assistant research scientist in the department of biochemistry and molecular biology, 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. The number of these cancer stem cells determines how rapidly the cancer will form and develop.
The research was supported by the National Institutes of Health.