"The team has shown that this biomechanical process is mediated by two proteins, FAK and paxillin, which act as mechanosensors of the stiffness of the surrounding tissue. If the interaction of these two molecules is blocked, cancer cells lose the ability to sense stiffness. The researchers grafted pancreatic tumors from human patients into mice and then blocked the interaction of the two proteins. This completely halted metastasis to other organs."
"We have seen that at the onset of metastasis, the first process that induces tumor migration is clearly durotaxis due to the rigidity of the cellular matrix, explains Lagares. When this process is interfered with by blocking the interaction of the two aforementioned proteins, the mechanical GPS is deactivated. The cells cannot leave the pancreas because durotaxis is not activated. The consequence is that metastasis to the liver is completely mitigated, he adds."
Increased stiffness around tumors forms rigid tissue structures that act as exit highways guiding cancer cells to other organs. This guidance process, durotaxis, is mediated by mechanosensing proteins FAK and paxillin that detect matrix rigidity. Blocking the interaction between FAK and paxillin prevents cells from sensing stiffness and disables durotaxis. In experiments grafting human pancreatic tumors into mice, inhibiting the FAK–paxillin interaction completely halted metastasis, including to the liver. An experimental drug, JP-153, has been identified that blocks the two proteins' interaction, offering a potential therapeutic strategy to prevent metastatic spread.
Read at english.elpais.com
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