E-cadherin: Unexpected actor of invadopodia formation in pancreatic cancer

E-cadherin is known as an epithelial marker often associated with tumour suppressive function. However, several studies revealed that some tumours cells, such as pancreatic cancer cells, with epithelial traits and high E-cadherin expression can undergo metastasis and form secondary tumours. These observations suggest an important role of E-cadherin in early stages of tumour cells invasion. Pancreatic ductal adenocarcinoma (PDAC) are highly metastatic with poor prognosis cancer and therefore provide an useful model to clarify E-cadherin function on tumour progression. To address the molecular function of E-cadherin regarding PDAC aggressivity, we knock-down E-cadherin expression in a pancreatic cancer cell line and analysed the consequences of E-cadherin depletion on the capacity of cells to form invasive structures called invadopodia. We then deciphered the molecular mechanisms by which E-cadherin regulates invadopodia formation by performing analysis of proteomes from control and E-cadh depleted cells.