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Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells
BACKGROUND: Lung cancer is the leading cause of cancer-related death in the world, with metastasis as the main reason for the mortality. CELF1 is an RNA-binding protein controlling the post-transcriptional regulation of genes related to cell survival. As yet, there is little knowledge of CELF1 expre...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3842801/ https://www.ncbi.nlm.nih.gov/pubmed/24237593 http://dx.doi.org/10.1186/1475-2867-13-115 |
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author | Wu, Li-Na Xue, Yi-Jun Zhang, Li-Jian Ma, Xue-Mei Chen, Jin-Feng |
author_facet | Wu, Li-Na Xue, Yi-Jun Zhang, Li-Jian Ma, Xue-Mei Chen, Jin-Feng |
author_sort | Wu, Li-Na |
collection | PubMed |
description | BACKGROUND: Lung cancer is the leading cause of cancer-related death in the world, with metastasis as the main reason for the mortality. CELF1 is an RNA-binding protein controlling the post-transcriptional regulation of genes related to cell survival. As yet, there is little knowledge of CELF1 expression and biological function in lung cancer. This study investigated the expression levels of CELF1 in lung cancer tissues and the biological function of CELF1 in lung cancer cells. METHODS: CELF1 mRNA expression was determined in lung cancer and normal tissues, and the relationship between the expression level of CELF1 and clinicopathological parameters was evaluated. The biological function of CELF1 in A549 and H1299 lung cancer cell lines growth was examined. RESULTS: The expression of CELF1 was higher in human lung cancer tissues compared with the normal lung tissue. Lentiviral-mediated transfection of CELF1 siRNA effectively silenced the expression of CELF1 in both A549 and H1299 cells. Moreover, CELF1 knockdown markedly reduced the survival rate of lung cancer cells. Colony formation assays revealed a reduction in the number and size of lung cancer cell colonies from CELF1 knockdown. CONCLUSION: These results indicated that CELF1 may have significant roles in the progression of lung cancer, and suggested that siRNA mediated silencing of CELF1 could be an effective tool in lung cancer treatment. |
format | Online Article Text |
id | pubmed-3842801 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-38428012013-11-29 Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells Wu, Li-Na Xue, Yi-Jun Zhang, Li-Jian Ma, Xue-Mei Chen, Jin-Feng Cancer Cell Int Primary Research BACKGROUND: Lung cancer is the leading cause of cancer-related death in the world, with metastasis as the main reason for the mortality. CELF1 is an RNA-binding protein controlling the post-transcriptional regulation of genes related to cell survival. As yet, there is little knowledge of CELF1 expression and biological function in lung cancer. This study investigated the expression levels of CELF1 in lung cancer tissues and the biological function of CELF1 in lung cancer cells. METHODS: CELF1 mRNA expression was determined in lung cancer and normal tissues, and the relationship between the expression level of CELF1 and clinicopathological parameters was evaluated. The biological function of CELF1 in A549 and H1299 lung cancer cell lines growth was examined. RESULTS: The expression of CELF1 was higher in human lung cancer tissues compared with the normal lung tissue. Lentiviral-mediated transfection of CELF1 siRNA effectively silenced the expression of CELF1 in both A549 and H1299 cells. Moreover, CELF1 knockdown markedly reduced the survival rate of lung cancer cells. Colony formation assays revealed a reduction in the number and size of lung cancer cell colonies from CELF1 knockdown. CONCLUSION: These results indicated that CELF1 may have significant roles in the progression of lung cancer, and suggested that siRNA mediated silencing of CELF1 could be an effective tool in lung cancer treatment. BioMed Central 2013-11-15 /pmc/articles/PMC3842801/ /pubmed/24237593 http://dx.doi.org/10.1186/1475-2867-13-115 Text en Copyright © 2013 Wu et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Primary Research Wu, Li-Na Xue, Yi-Jun Zhang, Li-Jian Ma, Xue-Mei Chen, Jin-Feng Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells |
title | Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells |
title_full | Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells |
title_fullStr | Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells |
title_full_unstemmed | Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells |
title_short | Si-RNA mediated knockdown of CELF1 gene suppressed the proliferation of human lung cancer cells |
title_sort | si-rna mediated knockdown of celf1 gene suppressed the proliferation of human lung cancer cells |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3842801/ https://www.ncbi.nlm.nih.gov/pubmed/24237593 http://dx.doi.org/10.1186/1475-2867-13-115 |
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