Fascin-dependent control of nuclear plasticity in invading cells

许多临床研究已经发现一种叫做束蛋白的蛋白质在人类乳腺癌中含量很高，但是人们对这种蛋白质是如何控制的知之甚少。该项目旨在研究控制束蛋白的因素，以及这种蛋白质如何促进乳腺癌细胞从原发肿瘤转移到远处的转移部位。当前知识的主要空白之一是对调节乳腺癌进展和转移的因素的详细了解。该项目将有助于识别可能导致癌细胞侵袭增加的新蛋白质，从而为设计未来的治疗方法提供新的可能靶点。本项目旨在研究乳腺癌细胞中控制束蛋白功能的因素，长期目的是破坏这一控制因素，防止癌细胞侵袭。我们将在实验室中使用人类乳腺癌细胞来研究促进这些细胞侵入类组织环境的不同蛋白质。然后，我们将使用不同的策略来抑制这些新发现的促进入侵的蛋白质。最终，这项研究可能会导致鉴定出导致乳腺癌侵入组织增加的新蛋白质。这对设计和开发预防乳腺癌转移的新药和治疗剂具有重要的参考价值。

Many clinical studies have identified a protein called fascin at high levels in human breast cancers, however very little is known about how this protein is controlled. This project aims to study the factors that control fascin and how this protein can promote movement of breast cancer cells away from primary tumours and into distant sites of metastases. One of the major gaps in current knowledge is a detailed understanding of the factors regulating breast cancer progression and metastasis. This project will help to identify new proteins that can lead to increased cancer cell invasion and therefore provide new possible targets for designing future treatments. This project aims to study the factors that control fascin function in breast cancer cells with the long-term aim of disrupting this controlling factor and preventing cancer cell invasion. We will use human breast cancer cells in the lab to study the different proteins that are responsible for promoting the invasion of these cells into tissue-like environments. We will then use different strategies to inhibit these newly identified invasion-promoting proteins. Ultimately this study could lead to the identification of new proteins that cause increased breast cancer invasion into tissues. This is very valuable information in the design and development of new drugs and therapeutic agents to prevent breast cancer metastasis.