Cancer Cells Spread Through The Body Via Adhesion Molecules

Connie K. Ho for — Your Universe Online

A new study from the Massachusetts Institute of Technology (MIT) has revealed that cancer cells break away from tumors via adhesion molecules, causing a spread of cancer throughout the body.

The findings from the research project were recently published in the journal Nature Communications and offer a glimpse into the possible development of cancer drug targets.

“As cancer cells become more metastatic, there can be a loss of adhesion to normal tissue structures. Then, as they become more aggressive, they gain the ability to stick to, and grow on, molecules that are not normally found in healthy tissues but are found in sites of tumor metastases,” remarked lead researcher Sangeeta Bhatia, a member of the David H. Koch Institute for Integrative Cancer Research at MIT, in a prepared statement. “If we can prevent them from growing at these new sites, we may be able to interfere with metastatic disease.”

According to the scientists, cells are usually attached to the extracellular matrix, a structural support system, in the body. The matrix assists in managing cellular behavior and the cells are held down with the help of integrins, a type of protein found on cell surfaces. These proteins let go of the cells when cancer cells metastasize.

In particular, the researchers looked at the adhesion properties of cancer cells from primary lung tumors that metastasized later, primary lung tumors that did not metastasize, metastatic tumors that moved to farther locations in the body, and metastatic tumors that moved to lymph nodes close by. Each type of cell was exposed to a different pair of molecules from the extracellular matrix. In particular, there was a pair of extracellular matrix molecules that were especially adhesive to fibronectin and galectin, which are made of proteins that attach to sugars. The scientists then recorded how the cells were attached to the protein pairs.

Based on the results of the project, the team of investigators believes that the technology can be utilized in future studies on cellular adhesion.

“They´ve not only scaled this up dramatically, they´re able to study the adhesion proteins in combination, which allows them to identify adhesion synergies,” noted Dr. Jan Pilch, an assistant professor at the University of Pittsburgh School of Medicine who is unaffiliated with the study, in the statement.

The team of investigators was surprised to discover that the cells from the metastatic tumors were similar to each other as opposed to similar to the cells of the primary tumor. Even though the metastatic cells are similar in adhesive qualities, they can move in different directions; some cells will change the mix of integrins expressed, while others will modify the sugars found on cell surfaces.

Past studies have shown that tumors can lead to metastasis as a result of the secretion of molecules that increases the growth of an environment that is conducive to cancer development. In particular, more galectin-3 is correlated with more aggressive metastasis. An increase in galectin-3 and other molecules that encourage tumor cells to grow may affect the process.

“There´s a lot of evidence to suggest that a hospitable niche for the tumor cells is being established prior to the cells even arriving and establishing a home there,” concluded the study´s lead author Nathan Reticker-Flynn, a doctoral student in Bhatia´s lab.

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