Journal
CANCER SCIENCE
Volume 108, Issue 11, Pages 2130-2141Publisher
WILEY
DOI: 10.1111/cas.13347
Keywords
Angiogenesis; DMKN; epithelial-mesenchymal transition; pancreatic ductal adenocarcinoma; STAT3
Categories
Funding
- Innovative Research Groups of the General Surgery of Wenzhou, Zhejiang, China [C20150003]
- Provinces and Ministries Co-Contribution of Zhejiang, China [wkj-zj-1706]
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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 ERK1/2 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.
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