癌症现在已成为全球主要死因之一。细胞因子和趋化因子分泌失衡已被报告与癌症发展有关。同时，CC趋化因子在癌症研究中受到了相当的关注。CCR10作为最新被鉴定的CC趋化因子受体（CCR），已被认为涉及了免疫细胞特别是淋巴细胞对上皮组织如皮肤的招募和浸润，通过与两种配体CCL27和CCL28的联结。除了稳态功能之外，已显示出几种机制会发生在肿瘤微环境中，失调CCR10/CCL27-CCL28的表达。因此，这些受体和配体在肿瘤微环境中介导T细胞的交通。根据招募的淋巴细胞类型，CCR10/CCL27-CCL28相互作用在癌症发展中发挥矛盾的作用。如果是T细胞助手、细胞毒性T细胞和自然杀伤细胞，则此轴的作用将是肿瘤抑制性的。相反，如果CCR10/CCL27-CCL28招募调节性T细胞、癌症相关成纤维细胞或骨髓源性抑制细胞，则会导致肿瘤进展。除了淋巴细胞和免疫细胞的交通外，CCR10还导致肿瘤细胞或内皮细胞（称为血管生成和淋巴管生成）的迁移，以促进肿瘤转移。此外，CCR10信号引发肿瘤促进信号，例如PI3K/AKT和有丝分裂原活化蛋白激酶/细胞外信号调节激酶，导致肿瘤细胞生长。由于CCR10/CCL27-CCL28在肿瘤组织中发生失调，因此建议分析和测量它们可能预测肿瘤发展。最后，希望基于这个轴的治疗方法可以增加我们对于克服肿瘤进展的认识。

Cancer is now one of the major causes of death across the globe. The imbalance of cytokine and chemokine secretion has been reported to be involved in cancer development. Meanwhile, CC chemokines have received considerable interest in cancer research. CCR10, as the latest identified CC chemokine receptor (CCR), has been implicated in the recruitment and infiltration of immune cells, especially lymphocytes, into epithelia such as skin via ligation to two ligands, CCL27 and CCL28. Other than homoeostatic function, several mechanisms have been shown to dysregulate CCR10/CCL27-CCL28 expression in the tumour microenvironment. As such, these receptors and ligands mediate T-cell trafficking in the tumour microenvironment. Depending on the types of lymphocytes recruited, CCR10/CCL27-CCL28 interaction has been shown to play conflicting roles in cancer development. If they were T helper and cytotoxic T cells and natural killer cells, the role of this axis would be tumour-suppressive. In contrast, if CCR10/CCL27-CCL28 recruited regulatory T cells, cancer-associated fibroblasts or myeloid-derived suppressor cells, it would lead to tumour progression. In addition to the trafficking of lymphocytes and immune cells, CCR10 also leads to the migration of tumour cells or endothelial cells (called angiogenesis and lymphangiogenesis) to promote tumour metastasis. Furthermore, CCR10 signalling triggers tumour-promoting signalling such as PI3K/AKT and mitogen-activated protein kinase/extracellular signal-regulated kinase, resulting in tumour cell growth. Since CCR10/CCL27-CCL28 is dysregulated in the tumour tissues, it is suggested that analysis and measurement of them might predict tumour development. Finally, it is hoped using therapeutic approaches based on this axis might increase our knowledge to overcome tumour progression.