This thesis deals with the process of epithelial-mesenchymal transition (EMT) and its relevance in cancer diagnosis and therapy. EMT is a complex process, in which epithelial cells shed their characteristics and acquire mesenchymal traits and functions. This transformation can occur in physiological processes, but it also plays a crucial role in cancer progression, metastasis and therapy resistance. The induction of EMT can have various different causes. Besides the tumor microenvironment, genetic and epigenetic alterations or DNA damage can also be responsible for inducing EMT. When it comes to DNA damage, mainly double-strand breaks, especially self-inflicted double-strand breaks, play a role in EMT induction. This mechanism, in which tumor cells cause double-strand breaks in their own DNA, has only recently been discovered. As a result of this kind of DNA damage, transcription factors like nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) are activated via complex signaling pathways. Apart from driving tumor growth, these are also known for inducing EMT. Altogether self-inflicted double-strand breaks lead to tumor progression and metastasis due to the cells’ transition to mesenchymal phenotypes. Because of its crucial role in cancer progression, EMT has become an interesting target for cancer diagnosis and treatment. Expression profiles of EMT markers could serve as a way to predict tumor metastasis. Targeting these markers might even prevent metastasis and therefore save patients’ lives.