Lymphovascular invasion (LVI) is associated with poor outcome in breast cancer (BC); however, its underlying mechanisms remain ill-defined. LVI in BC develops through complex molecular pathways involving not only the interplay with the surrounding microenvironment along with endothelial cells lining the lymphovascular spaces but also changes in the malignant epithelial cells with the acquisition of more invasive and migration abilities. In this review, we focus on the key features that enable tumour cell detachment from the primary niche, their migration and interaction with the surrounding microenvironment as well as the crosstalk with the vascular endothelial cells, which eventually lead to intravasation of tumour cells and LVI. Intravascular tumour cell survival and migration, their distant site extravasation, stromal invasion and growth are part of the metastatic cascade. Cancer cell migration commences with loss of tumour cells’ cohesion initiating the invasion and migration processes which are usually accompanied by the accumulation of specific cellular and molecular changes that enable tumour cells to overcome the blockades of the extracellular matrix, spread into surrounding tissues and interact with stromal cells and immune cells. Thereafter, tumour cells migrate further via interacting with lymphovascular endothelial cells to penetrate the vessel wall leading ultimately to intravasation of cancer cells. Exploring the potential factors influencing cell migration in LVI can help in understanding the underlying mechanisms of LVI to identify targeted therapy in BC.

中文翻译：

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淋巴血管侵袭的分子复杂性：细胞迁移在乳腺癌中的作用作为原型

淋巴血管浸润 (LVI) 与乳腺癌 (BC) 的不良预后有关；然而，其潜在机制仍然不明确。BC 中的 LVI 通过复杂的分子途径发展，不仅涉及与周围微环境以及淋巴血管空间内衬的内皮细胞的相互作用，而且还涉及恶性上皮细胞的变化，以获得更多的侵袭和迁移能力。在这篇综述中，我们关注使肿瘤细胞脱离主要生态位的关键特征，它们的迁移和与周围微环境的相互作用以及与血管内皮细胞的串扰，最终导致肿瘤细胞和 LVI 的血管内渗入。血管内肿瘤细胞的存活和迁移，它们的远处部位外渗，基质侵袭和生长是转移级联反应的一部分。癌细胞迁移开始于肿瘤细胞内聚力的丧失，启动侵袭和迁移过程，通常伴随着特定细胞和分子变化的积累，使肿瘤细胞能够克服细胞外基质的封锁，扩散到周围组织并与基质细胞和免疫细胞。此后，肿瘤细胞通过与淋巴血管内皮细胞相互作用而进一步迁移以穿透血管壁，最终导致癌细胞的内渗。探索影响 LVI 中细胞迁移的潜在因素有助于了解 LVI 的潜在机制，以确定 BC 中的靶向治疗。癌细胞迁移开始于肿瘤细胞内聚力的丧失，启动侵袭和迁移过程，通常伴随着特定细胞和分子变化的积累，使肿瘤细胞能够克服细胞外基质的封锁，扩散到周围组织并与基质细胞和免疫细胞。此后，肿瘤细胞通过与淋巴血管内皮细胞相互作用而进一步迁移以穿透血管壁，最终导致癌细胞的内渗。探索影响 LVI 中细胞迁移的潜在因素有助于了解 LVI 的潜在机制，以确定 BC 中的靶向治疗。癌细胞迁移开始于肿瘤细胞内聚力的丧失，启动侵袭和迁移过程，通常伴随着特定细胞和分子变化的积累，使肿瘤细胞能够克服细胞外基质的封锁，扩散到周围组织并与基质细胞和免疫细胞。此后，肿瘤细胞通过与淋巴血管内皮细胞相互作用而进一步迁移以穿透血管壁，最终导致癌细胞的内渗。探索影响 LVI 中细胞迁移的潜在因素有助于了解 LVI 的潜在机制，以确定 BC 中的靶向治疗。