Dermokine contributes to epithelial-mesenchymal transition through increased activation of signal transducer and activator of transcription 3 in pancreatic cancer.
Dermokine contributes to epithelial-mesenchymal transition through increased activation of signal transducer and activator of transcription 3 in pancreatic cancer.
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DOI：
10.1111/cas.13347
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发表时间：
2017-11
期刊：
影响因子：
5.7
通讯作者：
Zhou M
中科院分区：
文献类型：
--
作者：
Huang C;Xiang Y;Chen S;Yu H;Wen Z;Ye T;Sun H;Kong H;Li D;Yu D;Chen B;Zhou M
皮肤因子（DMKN）首先被发现与皮肤损伤愈合和皮肤癌有关。最近，它的表达与胰腺癌肿瘤发生有关，尽管其参与仍然知之甚少。在此，我们发现，在帕图-8988和PANC-1胰腺癌细胞系中，DMKN功能丧失导致信号转导和转录激活因子3的磷酸化减少，ERK 1/2和AKT丝氨酸/苏氨酸激酶的活化增加。这降低了胰腺导管腺癌（PDAC）细胞的增殖能力。此外，DMKN敲低降低了PDAC细胞的侵袭和迁移，部分逆转了上皮-间质转化，通过降低微血管密度延缓了异种移植动物模型中的肿瘤生长，并减弱了小鼠模型中人PDAC的远处转移。总之，这些数据表明DMKN可能是胰腺癌的潜在预后生物标志物和治疗靶点。
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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