Integrin α11 in pancreatic stellate cells regulates tumor stroma interaction in pancreatic cancer

What is it about?

Tumor cells undergo genetic alterations which results in their enormous proliferation and migration leading to tumor growth and metastasis. In recent years, it has become clear that tumor cells are not solely responsible for their behavior but the non-malignant cells in the tumor microenvironment play a major role here. These cells are called stromal cells and they secrete abundant factors which stimulate tumor cells (so called paracrine effect) and make them more aggressive for their growth but also for their migratory behavior. Pancreatic cancer is one of deadliest cancer types with only 8% survival rate and the tumor stroma interaction is a key characteristic of this tumor. One of the main cell types in the tumor stroma is fibroblasts which in pancreatic cancer derive from pancreatic stellate cells. In this study, we unravel the role of a specific receptor integrin alpha11 in controlling the stellate cells activation and their effect on tumor cells. We show that when we decrease alpha11 levels in stellate cells, these cells do not get activated. We also show that when the culture medium from stellate cells added to tumor cells they became more migratory. Intriguingly, the culture medium from stellate cells with decreased alpha11 were not able to activate tumor cell migration. With these data we demonstrate that alpha11 is a crucial receptor in stellate cells to control their paracrine effect on tumor cells and therefore is an important target for designing new medicine against pancreatic cancer.

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