SOX2 functions as a molecular rheostat to control the growth, tumorigenicity and drug responses of pancreatic ductal adenocarcinoma cells.

摘要: Pancreatic ductal adenocarcinoma (PDAC) is a highly deadly malignancy. Expression of the stem cell transcription factor SOX2 increases during progression PDAC. Knockdown in PDAC lines decreases growth vitro; whereas, stable overexpression one line reportedly vitro. Here, we reexamined role cells, because inducible other tumor types inhibits growth. In this study, four were engineered for or knockdown SOX2. Remarkably, cells vitro and reduces tumorigenicity. Additionally, vivo. Thus, tumorigenicity dependent on expression optimal levels - hallmark molecular rheostats. We also determined that alters responses to drugs used clinical trials. Increasing inhibition mediated by MEK AKT inhibitors; whereas further when are treated with these inhibitors. targeting SOX2, its mode action, could improve treatment