Reference - Detail
| RRC ID | 86137 |
|---|---|
| Author | Morishita H, Kawai K, Noda A, Egami Y, Araki N. |
| Title | Myosin-Ie drives ruffle-edge lamellipodia formation and motility in A549 invasive lung cancer cells. |
| Journal | Microscopy (Oxf) |
| Abstract |
Lamellipodia are generally defined as thin, sheet-like cell protrusions that constitute the actin cytoskeleton-based motile apparatus, which promotes the movement of migrating cells. Recently, we identified a novel type of lamellipodia, termed ruffle-edge lamellipodia, which have α-actinin-4 (ACTN4)-enriched multilayer membrane folds at their leading edges in certain invasive cancer cell lines. In this study, the role of unconventional myosin-Ie (Myo1E) in ACTN4-enriched ruffle-edge lamellipodia was analyzed using live-cell, immunofluorescence, and scanning electron microscopy. Immunofluorescence microscopy for endogenous Myo1E and live-cell imaging of mApple-Myo1E expressing cells showed that Myo1E was localized to ACTN4-rich lamellipodia tips in A549 cells. The wound healing assay and live-cell movies showed that Myo1E siRNA knockdown significantly suppressed cell migration and ruffle-edge lamellipodia formation. Furthermore, scanning electron microscopy demonstrated that Myo1E knockdown significantly reduced ruffle-edge structures. These results suggest that Myo1E may play an important role not only in the motility of ruffle-edge lamellipodia but also in the construction of ruffle-edge structures, which are probably associated with cancer cell invasion and metastasis. |
| Published | 2025-9-26 |
| DOI | 10.1093/jmicro/dfaf039 |
| PII | 8266491 |
| PMID | 41003730 |
| IF | 1.394 |
| Altmetric score |
オルトメトリクス指標項目
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| The most frequently cited source | News |
| Total number of mentions | 6 |
| Altmetric score changes over past 6months | 0.0 |
| Resource | |
| Human and Animal Cells | A549(RCB0098) |