Chemotaxis is a critical process in cancer progression, directing the movement of tumour and stromal cells in response to extracellular chemical gradients. This review summarizes how chemotaxis influences tumour cell and stromal cell behaviours, the molecular pathways regulating chemotaxis, and its role in shaping the tumour microenvironment and metastatic spread. Chemotaxis is essential for tumour dissemination, involving steps such as invasion, intravasation, extravasation, and growth at distant sites. Chemokines, chemokine receptors, growth factors, and their receptors mediate chemotaxis in tumour cells, with mutations or regulatory changes in these factors frequently involved in cancer development. Chemotaxis can lead to changes in cytoskeletal dynamics, enabling cell movement. Recent advances in technology and interdisciplinary research have provided new insights into chemotaxis mechanisms and potential therapeutic targets. Chemotaxis involves three steps: chemosensing, polarization, and locomotion. Tumour cells can migrate through amoeboid or mesenchymal modes, while collective migration involves groups of cells moving together. Different modes of migration are influenced by the tumour type and microenvironment. Chemotaxis is regulated by various pathways, including those involving G protein-coupled receptors (GPCRs), chemokine receptors, and growth factor receptors. The LEGI model describes how chemotactic signals are processed in tumour cells, with local excitation and global inhibition playing key roles. Chemotaxis is also influenced by factors such as cofilin, RHO GTPases, and the actin cytoskeleton. Chemokines and growth factors are key regulators of chemotaxis in tumour cells, with over 50 chemokines and receptors involved in cancer. CXCR4 and CXCL12 are important in metastasis, while EGF and other growth factors also play roles. Chemotaxis is crucial for tumour cell invasion and dissemination, with interactions between tumour cells and stromal cells, such as macrophages and fibroblasts, playing a significant role. Tumour cells can respond to shallow gradients, highlighting the importance of chemotaxis in metastasis. The presence of tumour microenvironment of metastasis (TMEM) is associated with distant organ metastasis. Therapeutic strategies targeting chemotaxis are being developed, including inhibitors of chemokine receptors and downstream effectors such as mTOR, PI3K, and SRC. Anti-angiogenic therapies, such as VEGF antagonists, are already in use. However, current therapies primarily focus on tumour growth rather than dissemination. New insights into chemotaxis and dissemination may lead to novel therapeutic endpoints. Anti-invasion and anti-dissemination therapies may require long-term treatment to prevent further spread. Despite challenges, chemotaxis remains a promising target for cancer therapy.Chemotaxis is a critical process in cancer progression, directing the movement of tumour and stromal cells in response to extracellular chemical gradients. This review summarizes how chemotaxis influences tumour cell and stromal cell behaviours, the molecular pathways regulating chemotaxis, and its role in shaping the tumour microenvironment and metastatic spread. Chemotaxis is essential for tumour dissemination, involving steps such as invasion, intravasation, extravasation, and growth at distant sites. Chemokines, chemokine receptors, growth factors, and their receptors mediate chemotaxis in tumour cells, with mutations or regulatory changes in these factors frequently involved in cancer development. Chemotaxis can lead to changes in cytoskeletal dynamics, enabling cell movement. Recent advances in technology and interdisciplinary research have provided new insights into chemotaxis mechanisms and potential therapeutic targets. Chemotaxis involves three steps: chemosensing, polarization, and locomotion. Tumour cells can migrate through amoeboid or mesenchymal modes, while collective migration involves groups of cells moving together. Different modes of migration are influenced by the tumour type and microenvironment. Chemotaxis is regulated by various pathways, including those involving G protein-coupled receptors (GPCRs), chemokine receptors, and growth factor receptors. The LEGI model describes how chemotactic signals are processed in tumour cells, with local excitation and global inhibition playing key roles. Chemotaxis is also influenced by factors such as cofilin, RHO GTPases, and the actin cytoskeleton. Chemokines and growth factors are key regulators of chemotaxis in tumour cells, with over 50 chemokines and receptors involved in cancer. CXCR4 and CXCL12 are important in metastasis, while EGF and other growth factors also play roles. Chemotaxis is crucial for tumour cell invasion and dissemination, with interactions between tumour cells and stromal cells, such as macrophages and fibroblasts, playing a significant role. Tumour cells can respond to shallow gradients, highlighting the importance of chemotaxis in metastasis. The presence of tumour microenvironment of metastasis (TMEM) is associated with distant organ metastasis. Therapeutic strategies targeting chemotaxis are being developed, including inhibitors of chemokine receptors and downstream effectors such as mTOR, PI3K, and SRC. Anti-angiogenic therapies, such as VEGF antagonists, are already in use. However, current therapies primarily focus on tumour growth rather than dissemination. New insights into chemotaxis and dissemination may lead to novel therapeutic endpoints. Anti-invasion and anti-dissemination therapies may require long-term treatment to prevent further spread. Despite challenges, chemotaxis remains a promising target for cancer therapy.