Suppression of mutant Kirsten-RAS (KRASG12D)-driven pancreatic carcinogenesis by dual-specificity MAP kinase phosphatases 5 and 6

• Published in: Oncogene Vol. 41; no. 20; pp. 2811 - 2823
• Main Authors: Kidger, Andrew M., Saville, Mark K., Rushworth, Linda K., Davidson, Jane, Stellzig, Julia, Ono, Motoharu, Kuebelsbeck, Ludwig A., Janssen, Klaus-Peter, Holzmann, Bernhard, Morton, Jennifer P., Sansom, Owen J., Caunt, Christopher J., Keyse, Stephen M.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 13.05.2022; Nature Publishing Group
• Subjects: 13; 13/51; 14; 42; 42/41; 631/67/395; 64; 64/60; 692/53/2423; 82; 82/29; 96; 96/106; Adenocarcinoma; Aging; Animal models; Animals; Apoptosis; Atrophy; Atrophy - pathology; Carcinogenesis; Carcinogenesis - genetics; Carcinogenesis - pathology; Carcinoma, Pancreatic Ductal - genetics; Carcinoma, Pancreatic Ductal - pathology; Cell Biology; Dual Specificity Phosphatase 6 - genetics; Dual-Specificity Phosphatases - genetics; Extracellular signal-regulated kinase; Human Genetics; Hyperplasia; Internal Medicine; MAP kinase; Medicine; Medicine & Public Health; Metaplasia; Metastases; Mice; Oncology; Pancreas - pathology; Pancreatic cancer; Pancreatic Neoplasms - genetics; Pancreatic Neoplasms - pathology; Phosphatase; Proto-Oncogene Proteins p21(ras) - genetics; Tumors; Weight Loss

The cytoplasmic phosphatase DUSP6 and its nuclear counterpart DUSP5 are negative regulators of RAS/ERK signalling. Here we use deletion of either Dusp5 or Dusp6 to explore the roles of these phosphatases in a murine model of KRAS G12D -driven pancreatic cancer. By 56-days, loss of either DUSP5 or DU...