Vimentin具有促进肿瘤侵袭和转移的作用。研究发现Bcl-2高表达促进喉癌的发生发展，但机制未明。前期证实Bcl-2能促进喉癌的侵袭和转移，并诱导Vimentin表达。为此，我们提出如下科学假说："Bcl-2通过诱导Vimentin表达，促进喉癌侵袭和转移"。本项目拟采用过表达或沉默Bcl-2观察对Vimentin表达和体内/外侵袭和转移的影响，从EMT相关转录因子和启动子等两个方面探讨诱导机制；观察过表达或沉默Vimentin对喉癌体内/外侵袭和转移的影响，并用串联亲和纯化耦联质谱技术为主的靶向蛋白质组学技术分离、鉴定喉癌细胞中Vimentin相互作用蛋白，研究Vimentin与其相互作用蛋白作用时动态分子网络的改变对Src和PI3K-AKT等信号通路和喉癌侵袭转移的影响，从而阐明Bcl-2通过Vimentin促进喉癌侵袭和转移的分子机理，为喉癌的靶向和个体化治疗提供新的实验依据。

Vimentin has a role in promoting tumor invasion and metastasis. The research was reported that high expression of Bcl-2 promoted the occurrence and development of laryngeal cancer, however, the mechanism remained unclear. We preliminary confirmed that Bcl-2 could promote invasion and metastasis of laryngeal cancer and induce the expression of Vimentin. Therefor, we propose the following scientific hypothesis: "high expression of Bcl-2 can promote invasion and metastasis of laryngeal cancer by inducing the expression of Vimentin". The project intends to use the overexpression or silencing expression of Bcl-2 to observe the expression of Vimentin and the invasion and metastasis of laryngeal carcinoma in vivo and in vitro,and to explore the mechanism of induction from the two aspects of EMT-inducible transcription factors and promoter activity.We continue to observe invasion and metastasis of laryngeal carcinoma in vivo and in vitro by the overexpression or silencing Vimentin, to separate and identify the Vimentin-interacting protein in the laryngeal cancer cells by the tandem affinity purification-coupled mass spectrometry-based targeted proteomics technology, to detect whether Vimentin protein and its interacting protein have role in change of the dynamic molecular network to effect on signaling pathway of Src and PI3K-AKT and invasion and metastasis of laryngeal cancer, and ultimately to elucidate the molecular mechanism which Bcl-2 promoted invasion and metastasis in laryngeal cancer by the induction of Vimentin. We hope to provide new experimental basis for the targeted and individual therapy.