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E2A Predicts Prognosis of Colorectal Cancer Patients and Regulates Cancer Cell Growth by Targeting miR-320a
BACKGROUND AND OBJECTIVE: Transcriptional factor E2A is crucial for the normal development and differentiation of B and T lymphocytes. Dysregulation of E2A leads to leukemia and tumorigenesis of some solid tumors. The expression and clinical significance of E2A as well as its role in colorectal canc...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890311/ https://www.ncbi.nlm.nih.gov/pubmed/24454819 http://dx.doi.org/10.1371/journal.pone.0085201 |
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author | Huang, Ao Zhao, Hongchao Quan, Yingjun Jin, Runsen Feng, Bo Zheng, Minhua |
author_facet | Huang, Ao Zhao, Hongchao Quan, Yingjun Jin, Runsen Feng, Bo Zheng, Minhua |
author_sort | Huang, Ao |
collection | PubMed |
description | BACKGROUND AND OBJECTIVE: Transcriptional factor E2A is crucial for the normal development and differentiation of B and T lymphocytes. Dysregulation of E2A leads to leukemia and tumorigenesis of some solid tumors. The expression and clinical significance of E2A as well as its role in colorectal cancer (CRC) are still unknown. This study aims to assess E2A expression in CRC tissues, evaluate its prognosis value, and investigate its role in colon cancer cell growth. METHODS: E2A expression in CRC tissues and normal mucosa was detected by immunohistochemical staining; Kaplan-Meier survival curve and Cox regression model were used to evaluate the prognostic value of E2A. Lentivirus was used to construct E2A stably knocked-down cells. MTT assay was employed to detect cell proliferation change; cell cycle was analyzed by flow cytometry; and chromatin immunoprecipitation (ChIP) assay was used to validate the predicted binding target of E2A. RESULTS: Expression of E2A was lower in CRC tissues than normal mucosa; low E2A expression correlated with advanced TNM stage and larger tumor size, and predicted poor prognosis of CRC patients. E2A knockdown resulted in increased cell proliferation rate and cell cycle acceleration. ChIP assay showed miR-320a was a direct target of E2A and upregulation of miR-320a in E2A downregulated cells could reverse cell proliferation and cell cycle changes caused by E2A deficiency. CONCLUSIONS: E2A is an independent prognostic factor for CRC patients and targets miR-320a to regulate cell proliferation of colon cancer cells. |
format | Online Article Text |
id | pubmed-3890311 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-38903112014-01-21 E2A Predicts Prognosis of Colorectal Cancer Patients and Regulates Cancer Cell Growth by Targeting miR-320a Huang, Ao Zhao, Hongchao Quan, Yingjun Jin, Runsen Feng, Bo Zheng, Minhua PLoS One Research Article BACKGROUND AND OBJECTIVE: Transcriptional factor E2A is crucial for the normal development and differentiation of B and T lymphocytes. Dysregulation of E2A leads to leukemia and tumorigenesis of some solid tumors. The expression and clinical significance of E2A as well as its role in colorectal cancer (CRC) are still unknown. This study aims to assess E2A expression in CRC tissues, evaluate its prognosis value, and investigate its role in colon cancer cell growth. METHODS: E2A expression in CRC tissues and normal mucosa was detected by immunohistochemical staining; Kaplan-Meier survival curve and Cox regression model were used to evaluate the prognostic value of E2A. Lentivirus was used to construct E2A stably knocked-down cells. MTT assay was employed to detect cell proliferation change; cell cycle was analyzed by flow cytometry; and chromatin immunoprecipitation (ChIP) assay was used to validate the predicted binding target of E2A. RESULTS: Expression of E2A was lower in CRC tissues than normal mucosa; low E2A expression correlated with advanced TNM stage and larger tumor size, and predicted poor prognosis of CRC patients. E2A knockdown resulted in increased cell proliferation rate and cell cycle acceleration. ChIP assay showed miR-320a was a direct target of E2A and upregulation of miR-320a in E2A downregulated cells could reverse cell proliferation and cell cycle changes caused by E2A deficiency. CONCLUSIONS: E2A is an independent prognostic factor for CRC patients and targets miR-320a to regulate cell proliferation of colon cancer cells. Public Library of Science 2014-01-13 /pmc/articles/PMC3890311/ /pubmed/24454819 http://dx.doi.org/10.1371/journal.pone.0085201 Text en © 2014 Huang et al http://creativecommons.org/licenses/by/4.0/ 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 properly credited. |
spellingShingle | Research Article Huang, Ao Zhao, Hongchao Quan, Yingjun Jin, Runsen Feng, Bo Zheng, Minhua E2A Predicts Prognosis of Colorectal Cancer Patients and Regulates Cancer Cell Growth by Targeting miR-320a |
title | E2A Predicts Prognosis of Colorectal Cancer Patients and Regulates Cancer Cell Growth by Targeting miR-320a |
title_full | E2A Predicts Prognosis of Colorectal Cancer Patients and Regulates Cancer Cell Growth by Targeting miR-320a |
title_fullStr | E2A Predicts Prognosis of Colorectal Cancer Patients and Regulates Cancer Cell Growth by Targeting miR-320a |
title_full_unstemmed | E2A Predicts Prognosis of Colorectal Cancer Patients and Regulates Cancer Cell Growth by Targeting miR-320a |
title_short | E2A Predicts Prognosis of Colorectal Cancer Patients and Regulates Cancer Cell Growth by Targeting miR-320a |
title_sort | e2a predicts prognosis of colorectal cancer patients and regulates cancer cell growth by targeting mir-320a |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890311/ https://www.ncbi.nlm.nih.gov/pubmed/24454819 http://dx.doi.org/10.1371/journal.pone.0085201 |
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