Membrane-binding Protein Regulates Cell Motility by Sensing Membrane Tension

In migrating cells, FBP17 localized to short membrane invaginations at the leading edge, while diminishing from the cell rear in response to plasma membrane tension increase. Conversely, following reduced plasma membrane tension, FBP17 dots randomly distributed throughout the cell, correlating with loss of polarized actin assembly on plasma membrane tension reduction.

In vitro experiments showed that FBP17 membrane-bending activity depended on liposomal membrane tension. Thus, FBP17 was the local activator of actin polymerization that was inhibited by plasma membrane tension in the feedback loop that regulated cell migration. The disruption of cell motility-regulating mechanisms has been cited as a key factor in cancer cell metastasis.

Senior author Dr. Toshiki Itoh, professor of biomedical science at Kobe University, said, "We are promoting research from a less studied perspective to identify new approaches to cancer treatment."

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