author_facet Li, Hui
Ma, Xuhui
Yang, Desheng
Suo, Zhimin
Dai, Rujiang
Liu, Chunhong
Li, Hui
Ma, Xuhui
Yang, Desheng
Suo, Zhimin
Dai, Rujiang
Liu, Chunhong
author Li, Hui
Ma, Xuhui
Yang, Desheng
Suo, Zhimin
Dai, Rujiang
Liu, Chunhong
spellingShingle Li, Hui
Ma, Xuhui
Yang, Desheng
Suo, Zhimin
Dai, Rujiang
Liu, Chunhong
Journal of Cellular Biochemistry
PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
Cell Biology
Molecular Biology
Biochemistry
author_sort li, hui
spelling Li, Hui Ma, Xuhui Yang, Desheng Suo, Zhimin Dai, Rujiang Liu, Chunhong 0730-2312 1097-4644 Wiley Cell Biology Molecular Biology Biochemistry http://dx.doi.org/10.1002/jcb.29370 <jats:title>Abstract</jats:title><jats:p>The aim of this study was to investigate the functional role and the underlying molecular mechanism of long noncoding RNA (lncRNA) prostate cancer–associated transcript 1 (PCAT‐1) in cisplatin resistance of gastric cancer (GC). Our results indicated that PCAT‐1 was overexpressed in CDDP‐resistant GC tumor tissues and cell lines. High expression of PCAT‐1 was closely correlated with short overall survival in patients with GC. Downregulation of PCAT‐1 resensitized CDDP‐resistant GC cells to cisplatin. In addition, PCAT‐1 epigenetically silenced PTEN through binding to the histone methyltransferase enhancer of zeste homolog 2 (EZH2), thus increasing H3K27me3. More importantly, PTEN silencing counteracted PCAT‐1 knockdown–mediated enhancement in cisplatin sensitivity of CDDP‐resistant GC cells. In summary, PCAT‐1 led to cisplatin resistance in GC cells through epigenetically suppressing PTEN expression, providing a novel therapeutic strategy for GC patients with chemoresistance.</jats:p> PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2 Journal of Cellular Biochemistry
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series Journal of Cellular Biochemistry
source_id 49
title PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_unstemmed PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_full PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_fullStr PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_full_unstemmed PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_short PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_sort pcat‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing pten via recruiting ezh2
topic Cell Biology
Molecular Biology
Biochemistry
url http://dx.doi.org/10.1002/jcb.29370
publishDate 2020
physical 1353-1361
description <jats:title>Abstract</jats:title><jats:p>The aim of this study was to investigate the functional role and the underlying molecular mechanism of long noncoding RNA (lncRNA) prostate cancer–associated transcript 1 (PCAT‐1) in cisplatin resistance of gastric cancer (GC). Our results indicated that PCAT‐1 was overexpressed in CDDP‐resistant GC tumor tissues and cell lines. High expression of PCAT‐1 was closely correlated with short overall survival in patients with GC. Downregulation of PCAT‐1 resensitized CDDP‐resistant GC cells to cisplatin. In addition, PCAT‐1 epigenetically silenced PTEN through binding to the histone methyltransferase enhancer of zeste homolog 2 (EZH2), thus increasing H3K27me3. More importantly, PTEN silencing counteracted PCAT‐1 knockdown–mediated enhancement in cisplatin sensitivity of CDDP‐resistant GC cells. In summary, PCAT‐1 led to cisplatin resistance in GC cells through epigenetically suppressing PTEN expression, providing a novel therapeutic strategy for GC patients with chemoresistance.</jats:p>
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author Li, Hui, Ma, Xuhui, Yang, Desheng, Suo, Zhimin, Dai, Rujiang, Liu, Chunhong
author_facet Li, Hui, Ma, Xuhui, Yang, Desheng, Suo, Zhimin, Dai, Rujiang, Liu, Chunhong, Li, Hui, Ma, Xuhui, Yang, Desheng, Suo, Zhimin, Dai, Rujiang, Liu, Chunhong
author_sort li, hui
container_issue 2
container_start_page 1353
container_title Journal of Cellular Biochemistry
container_volume 121
description <jats:title>Abstract</jats:title><jats:p>The aim of this study was to investigate the functional role and the underlying molecular mechanism of long noncoding RNA (lncRNA) prostate cancer–associated transcript 1 (PCAT‐1) in cisplatin resistance of gastric cancer (GC). Our results indicated that PCAT‐1 was overexpressed in CDDP‐resistant GC tumor tissues and cell lines. High expression of PCAT‐1 was closely correlated with short overall survival in patients with GC. Downregulation of PCAT‐1 resensitized CDDP‐resistant GC cells to cisplatin. In addition, PCAT‐1 epigenetically silenced PTEN through binding to the histone methyltransferase enhancer of zeste homolog 2 (EZH2), thus increasing H3K27me3. More importantly, PTEN silencing counteracted PCAT‐1 knockdown–mediated enhancement in cisplatin sensitivity of CDDP‐resistant GC cells. In summary, PCAT‐1 led to cisplatin resistance in GC cells through epigenetically suppressing PTEN expression, providing a novel therapeutic strategy for GC patients with chemoresistance.</jats:p>
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spelling Li, Hui Ma, Xuhui Yang, Desheng Suo, Zhimin Dai, Rujiang Liu, Chunhong 0730-2312 1097-4644 Wiley Cell Biology Molecular Biology Biochemistry http://dx.doi.org/10.1002/jcb.29370 <jats:title>Abstract</jats:title><jats:p>The aim of this study was to investigate the functional role and the underlying molecular mechanism of long noncoding RNA (lncRNA) prostate cancer–associated transcript 1 (PCAT‐1) in cisplatin resistance of gastric cancer (GC). Our results indicated that PCAT‐1 was overexpressed in CDDP‐resistant GC tumor tissues and cell lines. High expression of PCAT‐1 was closely correlated with short overall survival in patients with GC. Downregulation of PCAT‐1 resensitized CDDP‐resistant GC cells to cisplatin. In addition, PCAT‐1 epigenetically silenced PTEN through binding to the histone methyltransferase enhancer of zeste homolog 2 (EZH2), thus increasing H3K27me3. More importantly, PTEN silencing counteracted PCAT‐1 knockdown–mediated enhancement in cisplatin sensitivity of CDDP‐resistant GC cells. In summary, PCAT‐1 led to cisplatin resistance in GC cells through epigenetically suppressing PTEN expression, providing a novel therapeutic strategy for GC patients with chemoresistance.</jats:p> PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2 Journal of Cellular Biochemistry
spellingShingle Li, Hui, Ma, Xuhui, Yang, Desheng, Suo, Zhimin, Dai, Rujiang, Liu, Chunhong, Journal of Cellular Biochemistry, PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2, Cell Biology, Molecular Biology, Biochemistry
title PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_full PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_fullStr PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_full_unstemmed PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_short PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
title_sort pcat‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing pten via recruiting ezh2
title_unstemmed PCAT‐1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2
topic Cell Biology, Molecular Biology, Biochemistry
url http://dx.doi.org/10.1002/jcb.29370