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. Author manuscript; available in PMC: 2018 Nov 1.
Published in final edited form as: Biomaterials. 2017 Sep 8;146:146–155. doi: 10.1016/j.biomaterials.2017.09.012

Figure 5. Memory-dependent migration is not regulated by proliferation or long-distance signal transmission.

Figure 5

Representative leading-edge tracks of monolayers of MCF10A cells after treatment with (a) 2mM thymidine, a proliferation inhibitor, and (d) 4mM EGTA, a calcium chelator, recorded for 12 hours (3 h interval) in the secondary ECM, with color-coding for migration speed. Arrows indicate direction of migration. (b) Average leading edge migration speed for proliferation-inhibited cells. Columns with dashed outline represent the migration speed for control untreated MCF10A cells. N>15. (c) Average spreading area of individual cells in the secondary ECM with and without proliferation inhibition. N>30. (e) Average leading edge migration speed for EGTA-treated cells. N>15. (f) Immunofluorescent staining for E-cadherin (green) and DAPI (blue) in untreated and EGTA-treated MCF10A cells showing dysfunctional cell-cell junctions after EGTA treatment. Scale bars = 100 μm. (g) After 3-day priming and additional 1 day of migration in the secondary ECM, the primary ECM region is entirely removed. Leading-edge migration speed in the secondary ECM (right panel) shows preservation of memory-dependent migration despite a complete loss of communication with the primary region. N>15. Horizontal brackets denote statistical significance, p<0.05. Error bars = SEM.