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Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells

OBJECTIVES: Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential tar...

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Autores principales: Ao, Nannan, Dai, Yingchu, Chen, Qianping, Feng, Yang, Yu, Jingping, Wang, Chang, Liu, Fenju, Li, Ming, Liu, Geng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6457034/
https://www.ncbi.nlm.nih.gov/pubmed/30961474
http://dx.doi.org/10.1177/1533033819842546
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author Ao, Nannan
Dai, Yingchu
Chen, Qianping
Feng, Yang
Yu, Jingping
Wang, Chang
Liu, Fenju
Li, Ming
Liu, Geng
author_facet Ao, Nannan
Dai, Yingchu
Chen, Qianping
Feng, Yang
Yu, Jingping
Wang, Chang
Liu, Fenju
Li, Ming
Liu, Geng
author_sort Ao, Nannan
collection PubMed
description OBJECTIVES: Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential target pathways. METHODS: Two human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. Cell viability, cell cycle distribution, and apoptosis after Bortezomib treatment was detected by Cell Counting Kit-8, flow cytometry, and Annexin V/propidium iodide staining, respectively. The genes targeted by Bortezomib were analyzed at the messenger RNA level by microarray chips and quantitative real-time polymerase chain reaction. RESULTS: The proliferation of human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. Bortezomib treatment led to G(2)/M arrest and apoptosis. Microarray chips revealed multiple signaling pathways targeted by Bortezomib, including proteasome, endoplasmic reticulum, Wnt-, and calcium-mediated pathway. The expression patterns of 4 representative genes UBD, CUL3, HDAC6, and GADD45A were verified by quantitative real-time polymerase chain reaction and showed consistency with the microarray assay. CONCLUSION: Bortezomib could suppress cell viability, cause G(2)/M arrest, and induce apoptosis in human esophageal cancer cells, with possible targets including UBD, CUL3, HDAC6, and GADD45A.
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spelling pubmed-64570342019-04-19 Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells Ao, Nannan Dai, Yingchu Chen, Qianping Feng, Yang Yu, Jingping Wang, Chang Liu, Fenju Li, Ming Liu, Geng Technol Cancer Res Treat Original Article OBJECTIVES: Bortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential target pathways. METHODS: Two human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. Cell viability, cell cycle distribution, and apoptosis after Bortezomib treatment was detected by Cell Counting Kit-8, flow cytometry, and Annexin V/propidium iodide staining, respectively. The genes targeted by Bortezomib were analyzed at the messenger RNA level by microarray chips and quantitative real-time polymerase chain reaction. RESULTS: The proliferation of human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. Bortezomib treatment led to G(2)/M arrest and apoptosis. Microarray chips revealed multiple signaling pathways targeted by Bortezomib, including proteasome, endoplasmic reticulum, Wnt-, and calcium-mediated pathway. The expression patterns of 4 representative genes UBD, CUL3, HDAC6, and GADD45A were verified by quantitative real-time polymerase chain reaction and showed consistency with the microarray assay. CONCLUSION: Bortezomib could suppress cell viability, cause G(2)/M arrest, and induce apoptosis in human esophageal cancer cells, with possible targets including UBD, CUL3, HDAC6, and GADD45A. SAGE Publications 2019-04-08 /pmc/articles/PMC6457034/ /pubmed/30961474 http://dx.doi.org/10.1177/1533033819842546 Text en © The Author(s) 2019 http://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Original Article
Ao, Nannan
Dai, Yingchu
Chen, Qianping
Feng, Yang
Yu, Jingping
Wang, Chang
Liu, Fenju
Li, Ming
Liu, Geng
Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells
title Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells
title_full Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells
title_fullStr Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells
title_full_unstemmed Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells
title_short Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells
title_sort genome-wide profiling of the toxic effect of bortezomib on human esophageal carcinoma epithelial cells
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6457034/
https://www.ncbi.nlm.nih.gov/pubmed/30961474
http://dx.doi.org/10.1177/1533033819842546
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