The EGFR-HSF1 axis accelerates the tumorigenesis of pancreatic cancer

Abstract Background Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant diseases because its non-symptomatic tumorigenesis. We previous found heat shock factor 1 (HSF1) was critical for PDAC progression and aim this study to clarified mechanisms on early activation HSF1 role in pancreatic cancer Methods The expression location human or mice tissues were examined by immunohistochemically staining. mainly used acinar cell 3-dimensional (3D) culture a spontaneous precancerous lesion mouse model called LSL-Kras G12D/+ ; Pdx1-Cre (KC) (and pancreatitis models derived from KC mice) explore pro-tumorigenesis vitro vivo. Bioinformatics molecular experiments underlying between epidermal growth receptor (EGFR). Results In study, we that pharmacological inhibition slowed initiation suppressed pancreatitis-induced formation lesion. Next, bioinformatics analysis revealed closely linked EGFR pathway also confirmed their parallel lesions. Besides, Indeed, demonstrated mediated tumorigenesis partly HSF1-dependent vitro. Conclusion Hence, concluded EGFR-HSF1 axis promoted cancer.