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

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 prog...

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Autores principales: Chen, Luguang, Ma, Chao, Bian, Yun, Shao, Chengwei, Wang, Tiegong, Li, Jing, Chong, Xiaodan, Su, Li, Lu, Jianping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762325/
https://www.ncbi.nlm.nih.gov/pubmed/29340057
http://dx.doi.org/10.18632/oncotarget.22794
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author Chen, Luguang
Ma, Chao
Bian, Yun
Shao, Chengwei
Wang, Tiegong
Li, Jing
Chong, Xiaodan
Su, Li
Lu, Jianping
author_facet Chen, Luguang
Ma, Chao
Bian, Yun
Shao, Chengwei
Wang, Tiegong
Li, Jing
Chong, Xiaodan
Su, Li
Lu, Jianping
author_sort Chen, Luguang
collection PubMed
description 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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spelling pubmed-57623252018-01-16 Aberrant expression of STYK1 and E-cadherin confer a poor prognosis for pancreatic cancer patients Chen, Luguang Ma, Chao Bian, Yun Shao, Chengwei Wang, Tiegong Li, Jing Chong, Xiaodan Su, Li Lu, Jianping Oncotarget Research Paper 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. Impact Journals LLC 2017-11-30 /pmc/articles/PMC5762325/ /pubmed/29340057 http://dx.doi.org/10.18632/oncotarget.22794 Text en Copyright: © 2017 Chen et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Chen, Luguang
Ma, Chao
Bian, Yun
Shao, Chengwei
Wang, Tiegong
Li, Jing
Chong, Xiaodan
Su, Li
Lu, Jianping
Aberrant expression of STYK1 and E-cadherin confer a poor prognosis for pancreatic cancer patients
title Aberrant expression of STYK1 and E-cadherin confer a poor prognosis for pancreatic cancer patients
title_full Aberrant expression of STYK1 and E-cadherin confer a poor prognosis for pancreatic cancer patients
title_fullStr Aberrant expression of STYK1 and E-cadherin confer a poor prognosis for pancreatic cancer patients
title_full_unstemmed Aberrant expression of STYK1 and E-cadherin confer a poor prognosis for pancreatic cancer patients
title_short Aberrant expression of STYK1 and E-cadherin confer a poor prognosis for pancreatic cancer patients
title_sort aberrant expression of styk1 and e-cadherin confer a poor prognosis for pancreatic cancer patients
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762325/
https://www.ncbi.nlm.nih.gov/pubmed/29340057
http://dx.doi.org/10.18632/oncotarget.22794
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