DNA tumour viruses promote tumour cell invasion and metastasis by deregulating the normal processes of cell adhesion and motility
Research output: Contribution to journal › Article
Approximately 15-20% of global cancer incidence is causally linked to viral infection, yet the low incidence of cancers in healthy infected individuals suggests that malignant conversion of virus-infected cells occurs after a long period as a result of additional genetic modifications. There are four families of viruses that are now documented to be involved in the development of human cancers which include members of the polyomavirus, hepadnavirus, papillomavirus and herpesvirus families. Although a number of these viruses are implicated in the aetiology of lymphomas or leukaemias, the vast majority are associated with malignancies of epithelial cells. In epithelial tissues, several classes of proteins are involved in maintaining tissue architecture, including those that promote cell-cell adhesion, and others, which mediate cell-matrix interactions. Proteins representative of all classes are frequently altered in malignant tumour cells that possess invasive and metastatic properties. Malignant tumour cells acquire mechanisms to degrade basement membranes and invade the underlying tissue. Many viruses encode proteins which engage signalling pathways that affect one or more of these mechanisms. It is believed that activation of these processes by chronic viral infection can, under certain circumstances, promote tumour cell invasion and metastasis. This review will take a brief look at the current knowledge of viral-induced alterations in cell motility and invasiveness in the context of tumour invasion and metastasis.
|Number of pages||21|
|Journal||European Journal of Cell Biology|
|Publication status||Published - 1 Sep 2008|
- tumour virus, cytoskeleton, invasiveness, motility, metastasis, integrins, adhesion, matrix metalloproteases