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Effect of CEACAM-1 knockdown in human colorectal cancer cells

Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM-1) is the major antigen of the CD66 cluster of granulocyte differentiation antigens. The present study aimed to assess the biological function of CEACAM-1 on the growth of human colorectal cancer (CRC) cells in vitro. Treatment of cul...

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Detalles Bibliográficos
Autores principales: Han, Zhong-Min, Huang, He-Mei, Sun, Yong-Wu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036324/
https://www.ncbi.nlm.nih.gov/pubmed/30008845
http://dx.doi.org/10.3892/ol.2018.8835
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author Han, Zhong-Min
Huang, He-Mei
Sun, Yong-Wu
author_facet Han, Zhong-Min
Huang, He-Mei
Sun, Yong-Wu
author_sort Han, Zhong-Min
collection PubMed
description Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM-1) is the major antigen of the CD66 cluster of granulocyte differentiation antigens. The present study aimed to assess the biological function of CEACAM-1 on the growth of human colorectal cancer (CRC) cells in vitro. Treatment of cultured CRC HCT-8 cells with CEACAM-1-specific siRNA successfully downregulated CEACAM-1 expression by 61% compared with control cells. The effects of CEACAM-1 downregulation on HCT-8 cell proliferation and apoptosis were then assessed via Cell Counting kit-8 assay and flow cytometry, respectively. The results demonstrated that siRNA-induced CEACAM-1 downregulation significantly inhibited proliferation and increased apoptosis, but had no significant effect on cell cycle progression in HCT-8 cells. Together, these results suggest that CEACAM-1 activity is critical to CRC growth, and thus, CEACAM-1 may be a promising therapeutic target for the treatment of CRC.
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spelling pubmed-60363242018-07-15 Effect of CEACAM-1 knockdown in human colorectal cancer cells Han, Zhong-Min Huang, He-Mei Sun, Yong-Wu Oncol Lett Articles Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM-1) is the major antigen of the CD66 cluster of granulocyte differentiation antigens. The present study aimed to assess the biological function of CEACAM-1 on the growth of human colorectal cancer (CRC) cells in vitro. Treatment of cultured CRC HCT-8 cells with CEACAM-1-specific siRNA successfully downregulated CEACAM-1 expression by 61% compared with control cells. The effects of CEACAM-1 downregulation on HCT-8 cell proliferation and apoptosis were then assessed via Cell Counting kit-8 assay and flow cytometry, respectively. The results demonstrated that siRNA-induced CEACAM-1 downregulation significantly inhibited proliferation and increased apoptosis, but had no significant effect on cell cycle progression in HCT-8 cells. Together, these results suggest that CEACAM-1 activity is critical to CRC growth, and thus, CEACAM-1 may be a promising therapeutic target for the treatment of CRC. D.A. Spandidos 2018-08 2018-05-30 /pmc/articles/PMC6036324/ /pubmed/30008845 http://dx.doi.org/10.3892/ol.2018.8835 Text en Copyright: © Han 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
Han, Zhong-Min
Huang, He-Mei
Sun, Yong-Wu
Effect of CEACAM-1 knockdown in human colorectal cancer cells
title Effect of CEACAM-1 knockdown in human colorectal cancer cells
title_full Effect of CEACAM-1 knockdown in human colorectal cancer cells
title_fullStr Effect of CEACAM-1 knockdown in human colorectal cancer cells
title_full_unstemmed Effect of CEACAM-1 knockdown in human colorectal cancer cells
title_short Effect of CEACAM-1 knockdown in human colorectal cancer cells
title_sort effect of ceacam-1 knockdown in human colorectal cancer cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036324/
https://www.ncbi.nlm.nih.gov/pubmed/30008845
http://dx.doi.org/10.3892/ol.2018.8835
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