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Molecular mechanisms of cancer cell invasion

Mortality among cancer patients rises sharply with the occurrence of distant organ metastases. The formation of these secondary neoplasms occurs in a stepwise process which is initiated when tumor cells begin to invade the surrounding tissue, detach from the primary tumor, disseminate via blood and lymphatic vessels, and eventually reach a secondary organ.

Our research activities concentrate on the earliest steps of the metastasis cascade, the penetration of the basement membrane and the local invasion of the underlying stromal tissue. These events are greatly facilitated when cancer cells are induced to undergo an epithelial-to-mesenchymal transition (EMT). EMT is a conserved cell biological program which results in the disruption of cell-cell and cell-matrix adhesion, the gain of motility and invasiveness, alterations in stemness, and therapy resistance.
  Figure 1: Emerging gene regulatory networks controlling epithelial and mesenchymal states of colorectal cancer cells.  
From a mechanistic perspective, EMT represents an extreme form of transcriptional reprogramming. Central to this process are the transcription factors SNAIL1, TWIST1 and ZEB1. However, the extent of EMT-associated gene expression changes reaches far beyond what can be explained solely by their activities. Moreover, it has become controversial whether cancer cells fully or only partially undergo EMT in order retain sufficient plasticity to revert to an epithelial phenotype at the metastatic site. For the molecular understanding of cancer cell invasion and metastasis it is therefore an important task to determine which signal transduction pathways and transcription factors control the generation, maintenance, and interconversion of gene expression programs that specify epithelial, mesenchymal, and intermediate epithelial/mesenchymal cancer cell states.
(Figure 1)
To investigate the gene regulatory networks that control the invasive behavior of cancer cells we apply cell biological techniques, molecular genetics, functional genomics, and bioinformatics, using human cell lines and genetically engineered murine intestinal organoids as model systems. Our long-term goal is to decisively advance our understanding of the molecular mechanisms operating in cancer cell invasion.
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