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Loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion
Cyclin‐dependent kinase‐like 2 (CDKL2), a new member of the cyclin‐dependent kinase family, may be involved in gastric cancer (GC) progression. Thus, we conducted this study to explore the clinical effect of CDKL2 in GC. Immunohistochemistry was used to measure CDKL2 levels in gastric tissues. The a...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6051174/ https://www.ncbi.nlm.nih.gov/pubmed/29790675 http://dx.doi.org/10.1002/cam4.1577 |
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author | Fang, Chia‐Lang Uen, Yih‐Huei Chen, Han‐Kun Hseu, You‐Cheng Lin, Chih‐Chan Hung, Shih‐Ting Sun, Ding‐Ping Lin, Kai‐Yuan |
author_facet | Fang, Chia‐Lang Uen, Yih‐Huei Chen, Han‐Kun Hseu, You‐Cheng Lin, Chih‐Chan Hung, Shih‐Ting Sun, Ding‐Ping Lin, Kai‐Yuan |
author_sort | Fang, Chia‐Lang |
collection | PubMed |
description | Cyclin‐dependent kinase‐like 2 (CDKL2), a new member of the cyclin‐dependent kinase family, may be involved in gastric cancer (GC) progression. Thus, we conducted this study to explore the clinical effect of CDKL2 in GC. Immunohistochemistry was used to measure CDKL2 levels in gastric tissues. The association of a high CDKL2 level with clinical and pathological characteristics, and the correlation between the CDKL2 level and disease‐free and overall survival were analyzed. Transfection was employed to overexpress CDKL2 in GC cells and to investigate the effect of CDKL2 overexpression on cell proliferation and invasion. Loss of CDKL2 was positively correlated with several clinical and pathological characteristics, and patients with a low CDKL2 level had significantly poorer disease‐free and overall survival than those with a high level (P = .005 and .001, respectively). Univariate analysis using the Cox proportional hazards model indicated that a low CDKL2 level was a prognosticator for inferior disease‐free survival (P = .007). Based on immmunoblotting data, AGS and HGC‐27 GC cells were chosen for CDKL2 overexpression. Cellular studies revealed that CDKL2 overexpression impaired cell proliferation and invasion. Loss of CDKL2 may serve as a biomarker for predicting GC patient outcomes and a potential therapeutic target for GC treatment. |
format | Online Article Text |
id | pubmed-6051174 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-60511742018-07-20 Loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion Fang, Chia‐Lang Uen, Yih‐Huei Chen, Han‐Kun Hseu, You‐Cheng Lin, Chih‐Chan Hung, Shih‐Ting Sun, Ding‐Ping Lin, Kai‐Yuan Cancer Med Clinical Cancer Research Cyclin‐dependent kinase‐like 2 (CDKL2), a new member of the cyclin‐dependent kinase family, may be involved in gastric cancer (GC) progression. Thus, we conducted this study to explore the clinical effect of CDKL2 in GC. Immunohistochemistry was used to measure CDKL2 levels in gastric tissues. The association of a high CDKL2 level with clinical and pathological characteristics, and the correlation between the CDKL2 level and disease‐free and overall survival were analyzed. Transfection was employed to overexpress CDKL2 in GC cells and to investigate the effect of CDKL2 overexpression on cell proliferation and invasion. Loss of CDKL2 was positively correlated with several clinical and pathological characteristics, and patients with a low CDKL2 level had significantly poorer disease‐free and overall survival than those with a high level (P = .005 and .001, respectively). Univariate analysis using the Cox proportional hazards model indicated that a low CDKL2 level was a prognosticator for inferior disease‐free survival (P = .007). Based on immmunoblotting data, AGS and HGC‐27 GC cells were chosen for CDKL2 overexpression. Cellular studies revealed that CDKL2 overexpression impaired cell proliferation and invasion. Loss of CDKL2 may serve as a biomarker for predicting GC patient outcomes and a potential therapeutic target for GC treatment. John Wiley and Sons Inc. 2018-05-23 /pmc/articles/PMC6051174/ /pubmed/29790675 http://dx.doi.org/10.1002/cam4.1577 Text en © 2018 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Clinical Cancer Research Fang, Chia‐Lang Uen, Yih‐Huei Chen, Han‐Kun Hseu, You‐Cheng Lin, Chih‐Chan Hung, Shih‐Ting Sun, Ding‐Ping Lin, Kai‐Yuan Loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion |
title | Loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion |
title_full | Loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion |
title_fullStr | Loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion |
title_full_unstemmed | Loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion |
title_short | Loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion |
title_sort | loss of cyclin‐dependent kinase‐like 2 predicts poor prognosis in gastric cancer, and its overexpression suppresses cells growth and invasion |
topic | Clinical Cancer Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6051174/ https://www.ncbi.nlm.nih.gov/pubmed/29790675 http://dx.doi.org/10.1002/cam4.1577 |
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