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Suppressed tumorigenicity of human endometrial cancer cells by the restored expression of the DCC gene
To obtain functional evidence for DCC as a tumour suppressor associated with endometrial cancer, the human DCC cDNA encoding a complete open reading frame (ORF) was transfected into highly tumorigenic human endometrial carcinoma cells, HHUA and Ishikawa in which DCC expression was completely deleted...
Autores principales: | , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2000
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2363268/ https://www.ncbi.nlm.nih.gov/pubmed/10646905 http://dx.doi.org/10.1054/bjoc.1999.0943 |
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author | Kato, H Zhou, Y Asanoma, K Kondo, H Yoshikawa, Y Watanabe, K Matsuda, T Wake, N Barrett, J C |
author_facet | Kato, H Zhou, Y Asanoma, K Kondo, H Yoshikawa, Y Watanabe, K Matsuda, T Wake, N Barrett, J C |
author_sort | Kato, H |
collection | PubMed |
description | To obtain functional evidence for DCC as a tumour suppressor associated with endometrial cancer, the human DCC cDNA encoding a complete open reading frame (ORF) was transfected into highly tumorigenic human endometrial carcinoma cells, HHUA and Ishikawa in which DCC expression was completely deleted. Reconstituted expression of DCC in HHUA had little effect on in vitro growth, but suppressed tumour formation in mice completely. The clones from Ishikawa had abundant DCC expression similar to that in normal endometrium. Their growth in vitro was suppressed and showed apoptotic phenotype. Lower levels of DCC expression in the prolonged passaged clones did not induce apoptosis, but still had the potential to suppress tumorigenicity. These observations imply a role of DCC in regulation of normal endometrial cell growth, and categorize DCC as the tumour suppressor gene for endometrial cancer. © 2000 Cancer Research Campaign |
format | Text |
id | pubmed-2363268 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2000 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-23632682009-09-10 Suppressed tumorigenicity of human endometrial cancer cells by the restored expression of the DCC gene Kato, H Zhou, Y Asanoma, K Kondo, H Yoshikawa, Y Watanabe, K Matsuda, T Wake, N Barrett, J C Br J Cancer Regular Article To obtain functional evidence for DCC as a tumour suppressor associated with endometrial cancer, the human DCC cDNA encoding a complete open reading frame (ORF) was transfected into highly tumorigenic human endometrial carcinoma cells, HHUA and Ishikawa in which DCC expression was completely deleted. Reconstituted expression of DCC in HHUA had little effect on in vitro growth, but suppressed tumour formation in mice completely. The clones from Ishikawa had abundant DCC expression similar to that in normal endometrium. Their growth in vitro was suppressed and showed apoptotic phenotype. Lower levels of DCC expression in the prolonged passaged clones did not induce apoptosis, but still had the potential to suppress tumorigenicity. These observations imply a role of DCC in regulation of normal endometrial cell growth, and categorize DCC as the tumour suppressor gene for endometrial cancer. © 2000 Cancer Research Campaign Nature Publishing Group 2000-01 2000-01-18 /pmc/articles/PMC2363268/ /pubmed/10646905 http://dx.doi.org/10.1054/bjoc.1999.0943 Text en Copyright © 2000 Cancer Research Campaign https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Regular Article Kato, H Zhou, Y Asanoma, K Kondo, H Yoshikawa, Y Watanabe, K Matsuda, T Wake, N Barrett, J C Suppressed tumorigenicity of human endometrial cancer cells by the restored expression of the DCC gene |
title | Suppressed tumorigenicity of human endometrial cancer cells by the restored expression of the DCC gene |
title_full | Suppressed tumorigenicity of human endometrial cancer cells by the restored expression of the DCC gene |
title_fullStr | Suppressed tumorigenicity of human endometrial cancer cells by the restored expression of the DCC gene |
title_full_unstemmed | Suppressed tumorigenicity of human endometrial cancer cells by the restored expression of the DCC gene |
title_short | Suppressed tumorigenicity of human endometrial cancer cells by the restored expression of the DCC gene |
title_sort | suppressed tumorigenicity of human endometrial cancer cells by the restored expression of the dcc gene |
topic | Regular Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2363268/ https://www.ncbi.nlm.nih.gov/pubmed/10646905 http://dx.doi.org/10.1054/bjoc.1999.0943 |
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