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Upregulation of the checkpoint protein CHFR is associated with tumor suppression in pancreatic cancers

The checkpoint with forkhead-associated (FHA) domain and RING-finger (CHFR) protein was identified as a cell cycle checkpoint protein and E3 ubiquitin ligase. In the present study, the potential functions of CHFR in pancreatic cancer were investigated. CHFR expression was measured in five pancreatic...

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Autores principales: Zhang, Di, Xu, Xiao-Lan, Li, Fei, Sun, Hai-Chen, Cui, Ye-Qing, Liu, Shuang, Xu, Ping-Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5755226/
https://www.ncbi.nlm.nih.gov/pubmed/29344247
http://dx.doi.org/10.3892/ol.2017.7239
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author Zhang, Di
Xu, Xiao-Lan
Li, Fei
Sun, Hai-Chen
Cui, Ye-Qing
Liu, Shuang
Xu, Ping-Yong
author_facet Zhang, Di
Xu, Xiao-Lan
Li, Fei
Sun, Hai-Chen
Cui, Ye-Qing
Liu, Shuang
Xu, Ping-Yong
author_sort Zhang, Di
collection PubMed
description The checkpoint with forkhead-associated (FHA) domain and RING-finger (CHFR) protein was identified as a cell cycle checkpoint protein and E3 ubiquitin ligase. In the present study, the potential functions of CHFR in pancreatic cancer were investigated. CHFR expression was measured in five pancreatic cancer cell lines by reverse transcription- quantitative polymerase chain reaction and western blotting. Capan-1 cells stably expressing CHFR were established by lentiviral vector transfection. Cell proliferation was assessed using Cell Counting Kit-8, and cell migration/invasion assay was determined using Transwell assays. Cell cycle and apoptosis induced by gemcitabine or docetaxel were evaluated using flow cytometry. CHFR expression levels were also evaluated in pancreatic ductal adenocarcinoma (PDAC) tumor samples as well as adjacent non-tumor tissues by immunohistochemistry. The significance of CHFR expression was determined, with respect to clinicopathological features and overall survival. Overexpression of CHFR in Capan-1 cells led to a decreased proliferative rate and reduced cell migration and invasion abilities. Results also indicated an increase in G1 phase cells in Capan-1 cells overexpressing CHFR. Docetaxel-induced apoptosis was inhibited in Capan-1 cells with CHFR-overexpression. A reduction in CHFR expression was detected in 51.9% of patients with PDAC, which significantly correlated with later T-stage. The results show CHFR functions as a tumor suppressor in pancreatic cancer, suggests its potential role in controlling the cell cycle of pancreatic cancer cells; however, CHFR overexpression is not a favorable factor in apoptosis induced by docetaxel.
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spelling pubmed-57552262018-01-17 Upregulation of the checkpoint protein CHFR is associated with tumor suppression in pancreatic cancers Zhang, Di Xu, Xiao-Lan Li, Fei Sun, Hai-Chen Cui, Ye-Qing Liu, Shuang Xu, Ping-Yong Oncol Lett Articles The checkpoint with forkhead-associated (FHA) domain and RING-finger (CHFR) protein was identified as a cell cycle checkpoint protein and E3 ubiquitin ligase. In the present study, the potential functions of CHFR in pancreatic cancer were investigated. CHFR expression was measured in five pancreatic cancer cell lines by reverse transcription- quantitative polymerase chain reaction and western blotting. Capan-1 cells stably expressing CHFR were established by lentiviral vector transfection. Cell proliferation was assessed using Cell Counting Kit-8, and cell migration/invasion assay was determined using Transwell assays. Cell cycle and apoptosis induced by gemcitabine or docetaxel were evaluated using flow cytometry. CHFR expression levels were also evaluated in pancreatic ductal adenocarcinoma (PDAC) tumor samples as well as adjacent non-tumor tissues by immunohistochemistry. The significance of CHFR expression was determined, with respect to clinicopathological features and overall survival. Overexpression of CHFR in Capan-1 cells led to a decreased proliferative rate and reduced cell migration and invasion abilities. Results also indicated an increase in G1 phase cells in Capan-1 cells overexpressing CHFR. Docetaxel-induced apoptosis was inhibited in Capan-1 cells with CHFR-overexpression. A reduction in CHFR expression was detected in 51.9% of patients with PDAC, which significantly correlated with later T-stage. The results show CHFR functions as a tumor suppressor in pancreatic cancer, suggests its potential role in controlling the cell cycle of pancreatic cancer cells; however, CHFR overexpression is not a favorable factor in apoptosis induced by docetaxel. D.A. Spandidos 2017-12 2017-10-20 /pmc/articles/PMC5755226/ /pubmed/29344247 http://dx.doi.org/10.3892/ol.2017.7239 Text en Copyright: © Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zhang, Di
Xu, Xiao-Lan
Li, Fei
Sun, Hai-Chen
Cui, Ye-Qing
Liu, Shuang
Xu, Ping-Yong
Upregulation of the checkpoint protein CHFR is associated with tumor suppression in pancreatic cancers
title Upregulation of the checkpoint protein CHFR is associated with tumor suppression in pancreatic cancers
title_full Upregulation of the checkpoint protein CHFR is associated with tumor suppression in pancreatic cancers
title_fullStr Upregulation of the checkpoint protein CHFR is associated with tumor suppression in pancreatic cancers
title_full_unstemmed Upregulation of the checkpoint protein CHFR is associated with tumor suppression in pancreatic cancers
title_short Upregulation of the checkpoint protein CHFR is associated with tumor suppression in pancreatic cancers
title_sort upregulation of the checkpoint protein chfr is associated with tumor suppression in pancreatic cancers
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5755226/
https://www.ncbi.nlm.nih.gov/pubmed/29344247
http://dx.doi.org/10.3892/ol.2017.7239
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