Good news! Cancer is history (soon)!
"the study builds on previous work in which the team found cells have an ability to sense the stiffness of their environment. This may be the rigid nature of bone material, the softer surroundings of fatty tissue or the medium stiffness of muscle tissue in between. This earlier research showed that the ability of cells to move differs between these environments. It also showed that there is a sweet spot for stiffness, in which the cells gain the best traction and can move at faster speeds. ...
The experiments deployed brain and breast cancer cells in between two environments, a stiffer region and a softer region, and the scientists observed for the first time that cells can actually gravitate towards the middle, which they describe as a "sweet spot." ...
From here, the team plans to develop a simulator that models how cancer cells move through a tumor. ..."
The experiments deployed brain and breast cancer cells in between two environments, a stiffer region and a softer region, and the scientists observed for the first time that cells can actually gravitate towards the middle, which they describe as a "sweet spot." ...
From here, the team plans to develop a simulator that models how cancer cells move through a tumor. ..."
From the abstract:
"How cells sense tissue stiffness to guide cell migration is a fundamental question in development, fibrosis and cancer. Although durotaxis—cell migration towards increasing substrate stiffness—is well established, it remains unknown whether individual cells can migrate towards softer environments. Here, using microfabricated stiffness gradients, we describe the directed migration of U-251MG glioma cells towards less stiff regions. This ‘negative durotaxis’ does not coincide with changes in canonical mechanosensitive signalling or actomyosin contractility. Instead, as predicted by the motor–clutch-based model, migration occurs towards areas of ‘optimal stiffness’, where cells can generate maximal traction. In agreement with this model, negative durotaxis is selectively disrupted and even reversed by the partial inhibition of actomyosin contractility. Conversely, positive durotaxis can be switched to negative by lowering the optimal stiffness by the downregulation of talin—a key clutch component. Our results identify the molecular mechanism driving context-dependent positive or negative durotaxis, determined by a cell’s contractile and adhesive machinery."
Directed cell migration towards softer environments (no public access)
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