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What are the molecular mechanisms underlying the regulation of metastasis by specific proteins in breast cancer? 


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The regulation of metastasis in breast cancer involves intricate molecular mechanisms. Firstly, breast cancer cells adapt to stressful environments through adaptive mutations, altered signaling pathways, and genetic alterations, leading to aggressive behavior and metastatic potential . Additionally, the expression of atypical chemokine receptor CCX-CKR acts as a decoy receptor, inhibiting breast cancer growth and metastasis by sequestering chemokines . Furthermore, the tumor microenvironment (TME) plays a crucial role in regulating metastasis through complex interactions involving multiple pathways like Hedgehog, Wnt, Notch, and NF-kB, which contribute to the aggressive nature of breast cancer progression and metastasis . Understanding these molecular interactions and pathways is essential for identifying potential therapeutic targets to combat breast cancer metastasis.

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Hedgehog, Wnt, Notch, and NF-kB pathways cross-regulate metastasis in breast cancer by influencing TME components, immune cells, EMT factors, and inflammatory genes, promoting aggressive metastatic progression.
Atypical chemokine receptor CCX-CKR inhibits breast cancer metastasis by sequestering chemokines, disrupting their interaction with G-protein-coupled receptors, thus impeding cancer growth and spread.
Open accessBook ChapterDOI
08 Mar 2023
Molecular mechanisms of breast cancer metastasis involve adaptive mutations, altered signaling pathways, and oncogene activation, leading to aggressive cell behavior and tissue invasion by heterogeneous cancer cells.
Atypical chemokine receptor CCX-CKR inhibits breast cancer metastasis by sequestering chemokines, acting as a decoy receptor. This mechanism hinders chemokine-mediated promotion of metastasis in breast cancer.

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