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Cancer cell invasion refers to the process by which malignant cells penetrate surrounding tissue barriers to enable local or distant spread (metastasis). It is a hallmark of cancer progression and involves changes in cell motility, adhesion, cytoskeletal dynamics, proteolytic degradation of the extracellular matrix (primarily mediated by matrix metalloproteinases and related enzymes), and signaling alterations such as those driven by epithelial-mesenchymal transition (EMT). Central molecules in invasion include integrins, actin cytoskeleton modulators (such as Rac1, Cdc42), and proteases (notably MMPs). Cancer cell invasion may occur via multiple patterns, including collective or individual cell migration[1][2][3][4][5]. Summary: "Cancer cell invasion" is not a molecular target, but a process involving multiple molecules (e.g., integrins, MMPs, actin regulators). For studies of drug mechanisms, specific molecular effectors (e.g., "matrix metalloproteinase-9", "integrin β1", "epidermal growth factor receptor") should be specified, as they are valid molecular targets within the invasion process.
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