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High expression of PDLIM5 facilitates cell tumorigenesis and migration by maintaining AMPK activation in prostate cancer
PDZ and LIM domain 5 (PDLIM5) is a cytoskeleton-associated protein and has been shown to bind to a variety of proteins through its specific domain, thereby acting to regulate cell migration and tumor progression. Here, we found that PDLIM5 was abnormally upregulated in prostate cancer (PCa) tissues...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716718/ https://www.ncbi.nlm.nih.gov/pubmed/29228678 http://dx.doi.org/10.18632/oncotarget.20981 |
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author | Liu, Xi Chen, Lu Huang, Hai Lv, Jian-Min Chen, Ming Qu, Fa-Jun Pan, Xiu-Wu Li, Lin Yin, Lei Cui, Xin-Gang Gao, Yi Xu, Dan-Feng |
author_facet | Liu, Xi Chen, Lu Huang, Hai Lv, Jian-Min Chen, Ming Qu, Fa-Jun Pan, Xiu-Wu Li, Lin Yin, Lei Cui, Xin-Gang Gao, Yi Xu, Dan-Feng |
author_sort | Liu, Xi |
collection | PubMed |
description | PDZ and LIM domain 5 (PDLIM5) is a cytoskeleton-associated protein and has been shown to bind to a variety of proteins through its specific domain, thereby acting to regulate cell migration and tumor progression. Here, we found that PDLIM5 was abnormally upregulated in prostate cancer (PCa) tissues as compared with that in normal prostate tissue. ONCOMINE microarray data mining showed that PDLIM5 was closely correlated with the prognosis of PCa in terms of Gleason score, tumor metastasis and biochemical recurrence. Lentivirus-mediated short hairpin RNA (shRNA) knockdown of PDLIM5 inhibited cell proliferation and colony formation, arrested hormone independent PCa cells DU145 and PC-3 in G2/M phase, and induced apoptosis. Meanwhile, silencing PDLIM5 inhibited migration and invasion of tumor cells by reversing the mesenchymal phenotype and a similar result was confirmed in a xenograft nude mouse model. Finally, we found PDLIM5 plays a crucial role in regulating malignant tumor cell proliferation, invasion and migration by binding to AMPK and affecting its activation and degradation, and may therefore prove to be a potential oncogenic gene in the development and progression of PCa. |
format | Online Article Text |
id | pubmed-5716718 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-57167182017-12-08 High expression of PDLIM5 facilitates cell tumorigenesis and migration by maintaining AMPK activation in prostate cancer Liu, Xi Chen, Lu Huang, Hai Lv, Jian-Min Chen, Ming Qu, Fa-Jun Pan, Xiu-Wu Li, Lin Yin, Lei Cui, Xin-Gang Gao, Yi Xu, Dan-Feng Oncotarget Research Paper PDZ and LIM domain 5 (PDLIM5) is a cytoskeleton-associated protein and has been shown to bind to a variety of proteins through its specific domain, thereby acting to regulate cell migration and tumor progression. Here, we found that PDLIM5 was abnormally upregulated in prostate cancer (PCa) tissues as compared with that in normal prostate tissue. ONCOMINE microarray data mining showed that PDLIM5 was closely correlated with the prognosis of PCa in terms of Gleason score, tumor metastasis and biochemical recurrence. Lentivirus-mediated short hairpin RNA (shRNA) knockdown of PDLIM5 inhibited cell proliferation and colony formation, arrested hormone independent PCa cells DU145 and PC-3 in G2/M phase, and induced apoptosis. Meanwhile, silencing PDLIM5 inhibited migration and invasion of tumor cells by reversing the mesenchymal phenotype and a similar result was confirmed in a xenograft nude mouse model. Finally, we found PDLIM5 plays a crucial role in regulating malignant tumor cell proliferation, invasion and migration by binding to AMPK and affecting its activation and degradation, and may therefore prove to be a potential oncogenic gene in the development and progression of PCa. Impact Journals LLC 2017-09-18 /pmc/articles/PMC5716718/ /pubmed/29228678 http://dx.doi.org/10.18632/oncotarget.20981 Text en Copyright: © 2017 Liu et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Research Paper Liu, Xi Chen, Lu Huang, Hai Lv, Jian-Min Chen, Ming Qu, Fa-Jun Pan, Xiu-Wu Li, Lin Yin, Lei Cui, Xin-Gang Gao, Yi Xu, Dan-Feng High expression of PDLIM5 facilitates cell tumorigenesis and migration by maintaining AMPK activation in prostate cancer |
title | High expression of PDLIM5 facilitates cell tumorigenesis and migration by maintaining AMPK activation in prostate cancer |
title_full | High expression of PDLIM5 facilitates cell tumorigenesis and migration by maintaining AMPK activation in prostate cancer |
title_fullStr | High expression of PDLIM5 facilitates cell tumorigenesis and migration by maintaining AMPK activation in prostate cancer |
title_full_unstemmed | High expression of PDLIM5 facilitates cell tumorigenesis and migration by maintaining AMPK activation in prostate cancer |
title_short | High expression of PDLIM5 facilitates cell tumorigenesis and migration by maintaining AMPK activation in prostate cancer |
title_sort | high expression of pdlim5 facilitates cell tumorigenesis and migration by maintaining ampk activation in prostate cancer |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716718/ https://www.ncbi.nlm.nih.gov/pubmed/29228678 http://dx.doi.org/10.18632/oncotarget.20981 |
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