Washington, May 13 (ANI): In a new study, scientists at Albert Einstein College of Medicine of Yeshiva University have unravelled a mechanism responsible for turning on and off a gene crucial to breast cancer spread.
Einstein scientists had previously discovered a gene called ZBP1 (zipcode binding protein 1), which helps cells to move, grow and organize spatially.
"ZBP1 is very active in the developing embryo but largely silent in adult tissues," said Dr Robert H. Singer, professor and co-chair of anatomy and structural biology and co-director of the Gruss-Lipper Biophotonics Center at Einstein.
This gene has been found active in several types of cancer, including breast, colorectal, and non-small cell lung cancers; but the gene is silenced in metastasizing cancer cells.
In the new study, Singer and another Einstein scientist, Dr John Condeelis sought to determine how ZBP1 gene is activated and silenced and how it influences the spread of breast cancer.
The find may offer potential drug targets for preventing metastasis.
After examining mouse, rat, and human breast cancer cells, they found that ZBP1 silencing occurs when a methyl group (CH3) attaches to ZBP1's promoter region (the segment of a gene where gene expression is initiated).
The attachment of CH3 prevents the promoter from binding to a protein called beta-catenin. And without beta-catenin, the ZBP1 gene is effectively silenced.
The study showed that the silencing of ZBP1 increases cancer cells' ability to migrate and promotes the proliferation of metastatic cells.
The researchers claim that the study has important implications for forecasting breast cancer outcomes.
They said that signs of ZBP1 silencing in breast cancer cells would indicate that a breast tumour is likely to spread information that would help in choosing a treatment strategy.
"If you could turn on this protein in cancer cells, or prevent it from being turned off, you could seriously reduce the ability of the cells to metastasize," said Singer.
The study appears in the Journal of Cell Science. (ANI)