Polo-like kinase 1, PLK1, has important functions in maintaining genome stability and is involved in regulation of mitosis. PLK1 is up regulated in many invasive carcinomas. We asked whether it may also play a role in acquisition of invasiveness, a crucial step in transition to malignancy. In a model of metaplastic basal-like breast carcinoma progression, we found that PLK1 expression is necessary but not sufficient to induce invasiveness through laminin-rich extracellular matrix. PLK1 mediates invasion via Vimentin and {beta}1 integrin, both of which are necessary. We observed that PLK1 phosphorylates Vimentin on serine 82, which in turn regulates cell surface levels of {beta}1 integrin. We found PLK1 to be also highly expressed in pre-invasive in situ carcinomas of the breast. These results support a role for the involvement of PLK1 in the invasion process and point to this pathway as a potential therapeutic target for pre-invasive and invasive breast carcinoma treatment
