Cell’s mechanical changes nudge cancer

U. TEXAS-AUSTIN (US) — Mechanical property changes in cells may be responsible for the progression of cancer—a discovery that could pave the way for new ways to predict, treat, and prevent the disease.

To present a unique physics-based perspective, researchers devised a 3-D cancer model that shows that softening of cells and changes in cell binding cause cancerous behavior. These mechanical property changes cause cells to divide uncontrollably—making them less likely to die and resulting in malignant tumor growth.

“To date, cancer research has focused on biochemical factors,” says Parag Katira, a postdoctoral student at the University of Texas at Austin. “Instead of looking to solve numerous interdependent biochemical carcinogenic factors, we can now focus on a small number of mechanical factors. It’s a new approach.”


Cancers are caused by various genetic and carcinogenic factors, such as synthetic chemicals, radiation, the environment, and physical stress. However, there is an uncanny similarity in mechanical property changes, such as degree of stiffness and ability to bind to other cells, that differentiate healthy and cancerous cells, as previously observed for several types of cancers.

Cancer cells are softer than healthy cells, and when surrounded by stiffer, healthy cells, cancerous cells stay compact and don’t spread. When the number of neighboring cancerous cells increases, however, the resisting force from stiffer cells is lowered and softer cancerous cells relax and expand to cover a larger surface area. Stretching of cells increases their multiplication rate and lowers cells’ probability of death.

As reported in Physical Review Letters, the researchers’ computational model replicates the life cycle of cells within a tissue and is used to observe how mechanical property changes affect a cell’s behavior and fate within that tissue.

The team started with a completely healthy tissue where all the cells had the same stiffness and binding ability, and then softened a small cluster of cells at the center of the tissue. As long as the number of softened cells was less than a critical value, the tissue remained stable and healthy.

Past this threshold, there was an increase in the multiplication rate of softer cells compared with healthy, stiffer cells. Beyond this point, tumors grew by replacing surrounding healthy tissue and displayed clinically observed characteristics of malignant tumors.

The researchers also analyzed how a cell’s ability to bind, or stick, to other cells affected metastasis, or progression. They observed that changes in the inter-cellular binding ability of softened cells controlled the rate and form of growing tumors. They believe this model identifies a common physical mechanism by which various biochemical carcinogenic or genetic factors can drive cancer progression.

“We’re very excited about these results because they point to a unified understanding of cancer progression,” says Roger Bonnecaze, professor of chemical engineering. “This understanding opens up new avenues for attacking cancer.”

Researchers from Boston University contributed to the study.

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