我们对细胞迁移的速度和持久性如何影响肿瘤生长速率和大小的认识仍然不完整。为了解决这个问题，我们开发了一个数学模型，其中细胞在二维空间中迁移、分裂、死亡或进入血管内。通过探索广泛的速度和持久性组合，我们发现肿瘤生长与速度增加和更高的持久性呈正相关。作为一个生物学上相关的例子，我们聚焦于高尔基体破裂，这是一种经常与细胞迁移变化相关的现象。高尔基体破裂是通过巨噬因蛋白的耗竭引起的，下调与患者生存率相关。将巨噬因耗竭的乳腺癌细胞实验获得的迁移和侵袭特性应用于我们的数学模型，我们预测失去巨噬因会增加血管内的细胞数量。这个预测被验证，因为循环肿瘤细胞表达的巨噬因比原发肿瘤细胞显著减少。总之，我们的计算模型确定了调节肿瘤进展的细胞迁移特性，并揭示了巨噬因在乳腺癌进展中的作用。版权所有：©2023 Ghannoum等人。这是一篇开放获取文章，根据创作共用许可证发布，允许在任何媒介上无限制使用、分发和繁殖，只要原作者和出处被认可。

Our understanding of how speed and persistence of cell migration affects the growth rate and size of tumors remains incomplete. To address this, we developed a mathematical model wherein cells migrate in two-dimensional space, divide, die or intravasate into the vasculature. Exploring a wide range of speed and persistence combinations, we find that tumor growth positively correlates with increasing speed and higher persistence. As a biologically relevant example, we focused on Golgi fragmentation, a phenomenon often linked to alterations of cell migration. Golgi fragmentation was induced by depletion of Giantin, a Golgi matrix protein, the downregulation of which correlates with poor patient survival. Applying the experimentally obtained migration and invasion traits of Giantin depleted breast cancer cells to our mathematical model, we predict that loss of Giantin increases the number of intravasating cells. This prediction was validated, by showing that circulating tumor cells express significantly less Giantin than primary tumor cells. Altogether, our computational model identifies cell migration traits that regulate tumor progression and uncovers a role of Giantin in breast cancer progression.Copyright: © 2023 Ghannoum et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.