We therefore decided to conduct a comprehensive study on the putative role of Gal-3 in pancreatic cancer cells by analyzing in parallel the effect of transient silencing of Gal-3 in a panel of five well-established cell lines with high endogenous Gal-3 expression, as well as study the long-term effects of modulation of Gal-3 expression by stable knockdown in S2-007 cells (high endogenous Gal-3 expression) or stable overexpression in PaTu 8988t cells (negligible endogenous Gal-3 expression), respectively. Here, LGALS3 is linked to pancreatic neoplasm.