Abstract
BackgroundThe involvement of Wnt in carcinogenesis and progression of pancreatic cancer is currently intensely discussed. We evaluated activation of the Wnt signaling pathway by using a Wnt reporter mouse strain expressing β-galactosidase under the control of the Axin2 promotor during pancreatitis induced formation of precancerous lesions. We also evaluated activation of Wnt signaling during interaction of pancreatic cancer with the tumor stroma.ResultsActivation of Wnt signaling was observed during acinar-to-ductal metaplasia after chronic as well as acute pancreatitis. Activation of Wnt signaling was also noticed during growth of pancreatic cancer in an orthotopic syngeneic pancreas cancer model. Activation of Wnt signaling was, however, not observed in carcinoma associated fibroblasts, but was detected in few cell clusters inside the tumor. Genetic ablation of Axin2 significantly reduced body weight without having a major impact on blood glucose concentration. However, ablation of Axin2 had no influence on the observed β-galactosidase positive cell clusters or on tumor weight.ConclusionThese data demonstrate that the Wnt signaling pathway is activated during acinar-to-ductal metaplasia after injury to the pancreas. However these data do not support a major role of Wnt signaling or of Axin2 in carcinoma associated fibroblasts and tumor growth.Electronic supplementary materialThe online version of this article (doi:10.1186/s13578-016-0116-4) contains supplementary material, which is available to authorized users.
Highlights
The involvement of Wnt in carcinogenesis and progression of pancreatic cancer is currently intensely discussed
Dear Editor The expression of Axin2 is induced by canonical Wnt signaling during cancerogenesis and during many other Wnt-regulated physiological and pathophysiological processes [1]
In hepatocellular carcinoma 3 to 44 % of tumors contain mutations of CTNNB1 and 5 to 25 % contain mutations in AXIN1 resulting in activation of Wnt signaling [4]
Summary
The involvement of Wnt in carcinogenesis and progression of pancreatic cancer is currently intensely discussed. The introduction of the β-galactosidase gene into the locus of Axin2 in mice, generated a reporter strain (Axin2+/lacZ), which reliably expresses β-galactosidase in cells where Wnt signaling is activated [1]. In hepatocellular carcinoma 3 to 44 % of tumors contain mutations of CTNNB1 and 5 to 25 % contain mutations in AXIN1 resulting in activation of Wnt signaling [4].
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