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Science / Thu, 09 Jul 2026 The Times of India

Why tissues refuse to move, and how that matters for healing & cancer

Bengaluru: When you cut your skin, millions of cells must move together in a coordinated way to close the wound. During cancer, that same coordination can break down, allowing cells to spread. And when an embryo develops, tissues must carefully balance movement and stability to shape organs.A new study from IISc suggests that a hidden mechanical conversation between neighbouring cells helps determine how tissues behave. They predicted that tissues should become glass-like only when cells are inactive and packed extremely tightly. Instead of fluctuating over minutes, as seen in isolated cells, actin activity in these tissues rose and fell over roughly an hour.

Bengaluru

: When you cut your skin, millions of cells must move together in a coordinated way to close the wound. During cancer, that same coordination can break down, allowing cells to spread. And when an embryo develops, tissues must carefully balance movement and stability to shape organs.A new study from IISc suggests that a hidden mechanical conversation between neighbouring cells helps determine how tissues behave. The findings could improve scientists’ understanding of wound healing, cancer progression and embryonic development by showing that biology is driven not only by genes and chemicals, but also by physical forces.The study focuses on epithelial tissues, thin sheets of cells that cover the body’s surfaces and line internal organs. Although these tissues are made up of living, metabolically active cells, they often behave like glass, remaining rigid even while individual cells continue to function.Scientists have found similar behaviour in epithelial tissues, where some groups of cells become almost trapped and move very slowly while neighbouring cells remain mobile.This mix of slow and fast movement is a defining feature of glass-like materials.Existing theories could not explain this. They predicted that tissues should become glass-like only when cells are inactive and packed extremely tightly. But living tissues are constantly consuming energy, changing shape and generating forces, which should make them more fluid and allow cells to move freely.To understand this contradiction, IISc researchers combined lab experiments with computer simulations. Using time-lapse microscopy, they observed sheets of epithelial cells whose actin, a protein that controls cell shape and movement, had been tagged with fluorescent markers. The researchers tracked cell movement while also measuring the mechanical forces they exerted. Instead of fluctuating over minutes, as seen in isolated cells, actin activity in these tissues rose and fell over roughly an hour. “The first result that I got showed oscillation of actin levels over time. I spent a lot of time trying to understand where this hour-scale oscillation in actin is coming from,” says Sindhu Muthukrishnan, PhD student in the department of bioengineering and first author of the study.The answer, the researchers found, lay in neighbouring cells continually pushing and pulling on one another. Those mechanical interactions influence the organisation of actin, while actin in turn changes how cells generate force, creating a continuous feedback loop.“The mechanochemical feedback loop provides a new way of looking at things,” says Phanindra Dewan, PhD student in the department of physics and one of the study’s authors. The new model successfully recreated the glass-like behaviour seen in real tissues, showing that it emerges only when cellular crowding and this mechanochemical feedback act together.“Such feedback could explain similar behaviour in other tissues too,” says Medhavi Vishwakarma, assistant professor, department of bioengineering and corresponding author.“The study of cancer progression or disease emergence or embryonic development is not just a question about genetics or biochemistry but also a question about mechanics,” says Sumantra Sarkar, assistant professor, department of physics and corresponding author.

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