Dermokine contributes to epithelial-mesenchymal transition through increased activation of signal transducer and activator of transcription 3 in pancreatic cancer.
Chaohao HuangYukai XiangShengchuan ChenHuajun YuZhengde WenTingting YeHongwei SunHongru KongDapei LiDinglai YuBicheng ChenMengtao ZhouPublished in: Cancer science (2017)
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.
Keyphrases
- epithelial mesenchymal transition
- signaling pathway
- induced apoptosis
- protein kinase
- mouse model
- cell cycle arrest
- transforming growth factor
- endothelial cells
- cell proliferation
- pi k akt
- transcription factor
- poor prognosis
- soft tissue
- big data
- endoplasmic reticulum stress
- cell death
- oxidative stress
- lymph node
- long non coding rna
- risk assessment
- toll like receptor
- induced pluripotent stem cells
- data analysis
- pluripotent stem cells