The Wilms tumor suppressor gene (Wt1) encodes a zinc finger transcription factor. The factor is important in the development of gonads, kidneys, adrenals, spleen, and heart. Recent studies suggest that WT1 could also be playing physiological roles in adults.
    Latest findings have shown that under normal conditions, the Wtl gene is activated in stellate cells (a special type of repair cell present in the pancreas and kidney) after pancreatic injury, responsible for the repair process.
    Systemic deletion of WT1 in mice provokes a severe deterioration of the exocrine pancreas, with mesothelial disruption, E-cadherin downregulation, disorganization of acinar architecture and accumulation of ascitic transudate. Despite this extensive damage, pancreatic stellate cells do not become activated and lose their canonical markers.
    The researchers also observed that pharmacological induction of pancreatitis in normal mice provokes de novo expression of WT1 in pancreatic stellate cells, concomitant with their activation. When pancreatitis was induced in mice after WT1 ablation, pancreatic stellate cells expressed WT1 and became activated, leading to a partial rescue of the acinar structure and the quiescent pancreatic stellate cell population after recovery from pancreatitis.
    "If Wt1 is not activated, these cells will not be able to perform their functions," the researcher said, further pointing out that these cells play a key role in the progression of pancreatic cancer because they form alliances with tumor cells. Therefore, the results of this study indicate that the Wt1 gene is essential not only for the normal maintenance of the pancreas, but also for repair after pancreatic injury.”