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Tumor cell migration and invasion are the hallmark processes that enable the progression of localized cancer into systemic metastatic disease, which is responsible for the majority of cancer-related mortality [1, 14]. Migration involves the active movement of tumor cells through the interstitial space, while invasion refers to the penetration of surrounding tissues and the degradation of the extracellular matrix (ECM) by proteases such as matrix metalloproteinases (MMPs) [13, 15]. These processes are driven by complex signaling networks, including the epithelial-mesenchymal transition (EMT), and the formation of actin-rich protrusions called invadopodia [11, 16]. While 'tumor cell migration and invasion' is not a single molecular target, it is the primary focus for a class of drugs termed 'migrastatics,' which aim to inhibit metastasis by targeting components like integrins, Rho GTPases, and microtubules [1, 2]. Therapeutic development in this area faces significant challenges, including the functional plasticity of tumor cells and the essential role of these pathways in normal physiological functions such as wound healing and immune response [1, 14].
Diverse mechanisms including inhibition of matrix metalloproteinases, antagonism of chemokine receptors, blockade of integrin-mediated adhesion, and destabilization of the cytoskeleton.
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