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Dermokine ( DMKN ) was first identified in relation to skin lesion healing and skin carcinoma. Recently, its expression was associated with pancreatic cancer tumorigenesis, although its involvement remains poorly understood. Herein, we showed that  DMKN  loss of function in Patu‐8988 and  PANC ‐1 pancreatic cancer cell lines resulted in reduced phosphorylation of signal transducer and activator of transcription 3, and increased activation of  ERK 1/2 and  AKT  serine/threonine kinase. This decreased the proliferation ability of pancreatic ductal adenocarcinoma ( PDAC ) cells. In addition,  DMKN  knockdown decreased the invasion and migration of  PDAC  cells, partially reversed the epithelial–mesenchymal transition, retarded tumor growth in a xenograft animal model by decreasing the density of microvessels, and attenuated the distant metastasis of human  PDAC  in a mouse model. Taken together, these data suggested that  DMKN  could be a potential prognostic biomarker and therapeutic target in pancreatic cancer.

cancer science

Dermokine contributes to epithelial–mesenchymal transition through increased activation of signal transducer and activator of transcription 3 in pancreatic cancer