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Antitumor activity of curcumin is involved in down-regulation of YAP/TAZ expression in pancreatic cancer cells
Pancreatic cancer (PC) is one of the most aggressive human malignancies worldwide and is the fourth leading cause of cancer-related deaths. Curcumin (diferuloylmethane) is a polyphenol derived from the Curcuma longa plant. Certain studies have demonstrated that curcumin exerts its anti-tumor functio...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5346699/ https://www.ncbi.nlm.nih.gov/pubmed/27738325 http://dx.doi.org/10.18632/oncotarget.12596 |
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author | Zhou, Xiuxia Su, Jingna Feng, Shaoyan Wang, Lixia Yin, Xuyuan Yan, Jingzhe Wang, Zhiwei |
author_facet | Zhou, Xiuxia Su, Jingna Feng, Shaoyan Wang, Lixia Yin, Xuyuan Yan, Jingzhe Wang, Zhiwei |
author_sort | Zhou, Xiuxia |
collection | PubMed |
description | Pancreatic cancer (PC) is one of the most aggressive human malignancies worldwide and is the fourth leading cause of cancer-related deaths. Curcumin (diferuloylmethane) is a polyphenol derived from the Curcuma longa plant. Certain studies have demonstrated that curcumin exerts its anti-tumor function in a variety of human cancers including PC, via targeting multiple therapeutically important cancer signaling pathways. However, the detailed molecular mechanisms are not fully understood. Two transcriptional co-activators, YAP (Yes-associated protein) and its close paralog TAZ (transcriptional coactivator with PDZ-binding motif) exert oncogenic activities in various cancers. Therefore, in this study we aimed to determine the molecular basis of curcumin-induced cell proliferation inhibition in PC cells. First, we detected the anti-tumor effects of curcumin on PC cell lines using CTG assay, Flow cytometry, clonogenic assay, wound healing assay and Transwell invasion assay. We found that curcumin significantly suppressed cell growth, weakened clonogenic potential, inhibited migration and invasion, and induced apoptosis and cell cycle arrest in PC cells. We further measured that overexpression of YAP enhanced cell proliferation and abrogated the cytotoxic effects of curcumin on PC cells. Moreover, we found that curcumin markedly down-regulated YAP and TAZ expression and subsequently suppressed Notch-1 expression. Collectively, these findings suggest that pharmacological inhibition of YAP and TAZ activity may be a promising anticancer strategy for the treatment of PC patients. |
format | Online Article Text |
id | pubmed-5346699 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-53466992017-03-30 Antitumor activity of curcumin is involved in down-regulation of YAP/TAZ expression in pancreatic cancer cells Zhou, Xiuxia Su, Jingna Feng, Shaoyan Wang, Lixia Yin, Xuyuan Yan, Jingzhe Wang, Zhiwei Oncotarget Research Paper Pancreatic cancer (PC) is one of the most aggressive human malignancies worldwide and is the fourth leading cause of cancer-related deaths. Curcumin (diferuloylmethane) is a polyphenol derived from the Curcuma longa plant. Certain studies have demonstrated that curcumin exerts its anti-tumor function in a variety of human cancers including PC, via targeting multiple therapeutically important cancer signaling pathways. However, the detailed molecular mechanisms are not fully understood. Two transcriptional co-activators, YAP (Yes-associated protein) and its close paralog TAZ (transcriptional coactivator with PDZ-binding motif) exert oncogenic activities in various cancers. Therefore, in this study we aimed to determine the molecular basis of curcumin-induced cell proliferation inhibition in PC cells. First, we detected the anti-tumor effects of curcumin on PC cell lines using CTG assay, Flow cytometry, clonogenic assay, wound healing assay and Transwell invasion assay. We found that curcumin significantly suppressed cell growth, weakened clonogenic potential, inhibited migration and invasion, and induced apoptosis and cell cycle arrest in PC cells. We further measured that overexpression of YAP enhanced cell proliferation and abrogated the cytotoxic effects of curcumin on PC cells. Moreover, we found that curcumin markedly down-regulated YAP and TAZ expression and subsequently suppressed Notch-1 expression. Collectively, these findings suggest that pharmacological inhibition of YAP and TAZ activity may be a promising anticancer strategy for the treatment of PC patients. Impact Journals LLC 2016-10-12 /pmc/articles/PMC5346699/ /pubmed/27738325 http://dx.doi.org/10.18632/oncotarget.12596 Text en Copyright: © 2016 Zhou 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, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Zhou, Xiuxia Su, Jingna Feng, Shaoyan Wang, Lixia Yin, Xuyuan Yan, Jingzhe Wang, Zhiwei Antitumor activity of curcumin is involved in down-regulation of YAP/TAZ expression in pancreatic cancer cells |
title | Antitumor activity of curcumin is involved in down-regulation of YAP/TAZ expression in pancreatic cancer cells |
title_full | Antitumor activity of curcumin is involved in down-regulation of YAP/TAZ expression in pancreatic cancer cells |
title_fullStr | Antitumor activity of curcumin is involved in down-regulation of YAP/TAZ expression in pancreatic cancer cells |
title_full_unstemmed | Antitumor activity of curcumin is involved in down-regulation of YAP/TAZ expression in pancreatic cancer cells |
title_short | Antitumor activity of curcumin is involved in down-regulation of YAP/TAZ expression in pancreatic cancer cells |
title_sort | antitumor activity of curcumin is involved in down-regulation of yap/taz expression in pancreatic cancer cells |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5346699/ https://www.ncbi.nlm.nih.gov/pubmed/27738325 http://dx.doi.org/10.18632/oncotarget.12596 |
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