Research Papers:

Aberrant expression of STYK1 and E-cadherin confer a poor prognosis for pancreatic cancer patients

Luguang Chen, Chao Ma, Yun Bian, Chengwei Shao, Tiegong Wang, Jing Li, Xiaodan Chong, Li Su and Jianping Lu _

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Oncotarget. 2017; 8:111333-111345. https://doi.org/10.18632/oncotarget.22794

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Luguang Chen1,*, Chao Ma1,*, Yun Bian1, Chengwei Shao1, Tiegong Wang1, Jing Li1, Xiaodan Chong2, Li Su3 and Jianping Lu1

1Department of Radiology, Changhai Hospital of Shanghai, Second Military Medical University, Shanghai, China

2Cancer Institute, Institute of Translational Medicine, Second Military Medical University, Shanghai, China

3School of Pharmacy, Second Military Medical University, Shanghai, China

*These authors have contributed equally to this work

Correspondence to:

Jianping Lu, email: [email protected]

Li Su, email: [email protected]

Keywords: STYK1; E-cadherin; EMT; pancreatic cancer

Received: August 23, 2017     Accepted: November 14, 2017     Published: November 30, 2017


Previous studies showed that aberrant Serine/threonine/tyrosine kinase 1 (STYK1, also known as NOK) or/and E-cadherin were involved in the progression of some types of human cancers. However, whether they contributed to the development of pancreatic cancer was unknown. Here, we investigated the prognostic significance of aberrant STYK1 and E-cadherin in pancreatic cancer. Our results showed that STYK1 expression increased while E-cadherin decreased in pancreatic cancer tissues compared with normal pancreas tissues. STYK1 level was positively correlated with lymph node metastasis and clinical stage in pancreatic cancer patients. E-cadherin expression was inversely correlated with STYK1 expression in pancreatic cancer tissue samples. Patients with high STYK1 and low E-cadherin expression had the worst prognosis. In addition, STYK1 knockdown in pancreatic cancer cell lines inhibited cell proliferation, enhanced cell apoptosis, induced cell cycle arrest, and prohibited cell migration, while STYK1 over-expression showed the opposite effects. Silencing STYK1 also increased E-cadherin expression and inhibited epithelial-to-mesenchymal transition (EMT) and p-p38 expression in vitro. Over-expression had showed the opposite trends, and treatment with p38 inhibitor, SB203580, could reverse the trends. Thus, STYK1 repressed E-cadherin expression and promoted EMT, mediated by p38 MAPK signaling pathway, which was the possible mechanism for STYK1-mediated pancreatic cancer cell proliferation and migration. In summary, our results showed that STYK1 might be a prognostic marker for pancreatic cancer patients and might be a novel strategy for the treatment of pancreatic cancer.

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