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Cancer cell migration is a complex, multi-step process where cancer cells move from their primary site into surrounding tissues and vasculature, enabling invasion and metastasis[3][5][7]. This migration involves regulated cytoskeletal remodeling (primarily actin polymerization and myosin contractions), adhesion formation and turnover (via integrins and related proteins), and proteolytic degradation of the extracellular matrix (often through matrix metalloproteinases)[1][3][5]. Both single-cell (amoeboid, mesenchymal) and collective migration modes exist, reflecting remarkable plasticity in how cancer cells traverse diverse microenvironments[3][7]. The process is regulated by multiple signaling pathways, prominently Rho-family GTPases, EGFR/ERK/MAPK signaling, PI3K/Akt signaling, and intercellular cues from cancer-associated fibroblasts or extracellular matrix components[2][4][6][8]. Drug development focuses on inhibiting key nodes in these molecular networks rather than targeting "migration" itself. Thus, "cancer cell migration" is a cell behavior, not a singular molecular entity, protein, or receptor.
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