Open AccessDermokine contributes to epithelial–mesenchymal transition through increased activation of signal transducer and activator of transcription 3 in pancreatic cancer
Author(s) -
Huang Chaohao,
Xiang Yukai,
Chen Shengchuan,
Yu Huajun,
Wen Zhengde,
Ye Tingting,
Sun Hongwei,
Kong Hongru,
Li Dapei,
Yu Dinglai,
Chen Bicheng,
Zhou Mengtao
Publication year - 2017
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13347
Subject(s) - epithelial–mesenchymal transition , cancer research , pancreatic cancer , stat protein , carcinogenesis , protein kinase b , metastasis , gene knockdown , biology , mapk/erk pathway , signal transduction , pathology , medicine , cancer , stat3 , cell culture , microbiology and biotechnology , genetics
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.