Dysregulated cell movement is a hallmark of cancer progression and metastasis, the leading cause of cancer-related mortality. The metastatic cascade involves tumour cell migration, invasion, intravasation, dissemination, and colonisation of distant organs. These processes are influenced by reciprocal interactions between cancer cells and the tumour microenvironment (TME), including immune cells, stromal components, and extracellular matrix proteins. The epithelial–mesenchymal transition (EMT) plays a crucial role in providing cancer cells with invasive and stem-like properties, promoting dissemination and resistance to apoptosis. Conversely, the mesenchymal–epithelial transition (MET) facilitates metastatic colonisation and tumour re-initiation. Immune cells within the TME contribute to either anti-tumour response or immune evasion. These cells secrete cytokines, chemokines, and growth factors that shape the immune landscape and influence responses to immunotherapy. Notably, immune checkpoint blockade (ICB) has transformed cancer treatment, yet its efficacy is often dictated by the immune composition of the tumour site. Elucidating the molecular cross-talk between immune and cancer cells, identifying predictive biomarkers for ICB response, and developing strategies to convert cold tumours into immune-active environments is critical to overcoming resistance to immunotherapy and improving patient survival.
细胞运动失调是癌症进展和转移的标志,也是癌症相关死亡的主要原因。转移级联过程涉及肿瘤细胞的迁移、侵袭、内渗、播散及远端器官定植。这些过程受到癌细胞与肿瘤微环境(TME)之间相互作用的调控,包括免疫细胞、基质成分和细胞外基质蛋白。上皮-间质转化(EMT)通过赋予癌细胞侵袭性和类干细胞特性,在促进肿瘤播散和凋亡抵抗中发挥关键作用;而间质-上皮转化(MET)则有助于转移定植和肿瘤再起始。肿瘤微环境中的免疫细胞既可介导抗肿瘤反应,也可促进免疫逃逸。这些细胞通过分泌细胞因子、趋化因子和生长因子塑造免疫微环境,并影响免疫治疗应答。值得注意的是,免疫检查点阻断(ICB)虽已革新癌症治疗,但其疗效常受肿瘤部位免疫组成的影响。阐明免疫细胞与癌细胞间的分子互作机制,鉴定ICB应答的预测性生物标志物,并开发将"冷肿瘤"转化为免疫活性环境的策略,对于克服免疫治疗耐药性和提高患者生存率至关重要。