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New insights in cancer cell migration
By Mike Nagle, 14-May-2007
Related topics: Ingredients
A workshop being held this week in Italy has shed new light on how cancer cells spread around the body, highlighting new strategies for potentially combating the disease.
Researchers from the Institut Curie in France, the Weizmann Institute of Science in Israel and the Technischen Universitat in Germany teamed up to investigate the role of a certain protein called fascin in the spread of colorectal cancer.
"Cancer cells become metastatic because they acquire the ability to move and to invade other tissues. Like all the cells that able to move, this new behaviour relies on sensory organelles called filopodia that sense the environment and help the cells to decide where to go," explained Danijela Vignjevic from the Institute Curie, who presented the research at the Workshop on Cell Migration: from molecules to organisms and diseases, held in Milan.
"Fascin is a key component of filopodia, and, inside the colorectal cancer cells, it represents the target of a circuitry that leads to the activation of several genes."
The team discovered that as the tumour progresses, levels of fascin also increase. In vitro tests showed that it promotes cell migration and invasion, and in vivo experiments confirmed a link between the protein and metastasis.
Fascin plays a key role in the formation of a cell's scaffolding, which in turn affects how mobile it is. The scientists also noticed that once the tumour has spread to a secondary site, fascin is no longer active - once its job is done, its gene is turned off until it is needed again.
Vignjevic and colleagues now hope to generate a transgenic mouse model for colorectal cancer metastasis, which could provide further information into the mechanism of the disease.
However, one of the workshop organisers warned that, although it is tempting to speculate about future therapies, more investigation will be needed "before we can think of moving from bench to bedside".
A second presentation at the workshop highlighted how ovarian cancer cells respond to specific signals to begin migrating. Professor Denise Montell, at the Johns Hopkins University School of Medicine in Baltimore, US, explained that epithelial ovarian cancer develops in the ovary, especially in the cells that cover the outer surface of this organ and these cells are regulated by similar signals to tumour cells.
"Epithelial cells migrate in a way that is reminiscent of the migratory behaviour of cancer cells and this moving is highly coordinated as it responds to extracellular signals present in the surrounding microenvironment. Using our experimental model we were able to identify three kinds of signals," she said.
The team found that steroid hormones dictate the time when cells must start moving with growth factors pointing them in the right direction. Which cells acquire the ability to move depends on the actions of cytokines.
"Each of these signals must work together in order for the cells to proceed to their correct destination. But they are not the only ones," continued Prof Montell.
"We found that [the gene] Par-1 regulates the detachment of cells from the epithelium and a critical step in releasing the cells from the original tissue."
The findings may provide a base from which drug developers can design new therapies to treat ovarian cancer.
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