It has long been accepted that cells benefit from actin polymerization and actomyosin contractility when they migrate, as they give cells the flexibility they need to travel across cell matrices, says a Johns Hopkins University press release. But Johns Hopkins chemical and biomolecular engineering professor Konstantinos Konstantopoulos and his team have found that conventional wisdom doesn't mean much. In studying the way breast cancer cells migrate to form metastases, the team fashioned a microfluidic-based cell migration chamber with channels of different widths and containing an attractant at one end to induce the cells to travel across, the university says.
The results they got in one circumstance were expected: when the cells traveled across the 50 µm-wide channels, actin was evenly distributed over the surfaces of the cells; and when these cells were treated with drugs that inhibited actin polymerization and actomyosin contractility, the cells went nowhere. But when they looked at the 3 µm-wide channels, the researchers found actin only at the leading and trailing edges of the cells, and when these cells were also treated with drugs that inhibited actin polymerization and actomyosin contractility, they weren't inhibited in the same way as the cells traveling through wider channels, Johns Hopkins says.
"Actin polymerization and actomyosin contractility are critical for 2D cell migration but dispensable for migration through narrow channels," Konstantopoulos says. This kind of research elucidates how cancer cells migrate across heterogeneous environments, the university adds. Konstantopoulos' team is already planning to build another microfluidic device with bifurcated channels, with the aim of learning how cancer cells choose one path over another for migration.