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CircLMNB1 promotes colorectal cancer by regulating cell proliferation, apoptosis and epithelial-mesenchymal transition
OBJECTIVE: The aberrant expression of circular RNAs (circRNAs) is a frequent occurrence in various cancers. However, the functions and roles played by most circRNAs in colorectal cancer (CRC) remain largely unknown. MATERIALS AND METHODS: Levels of circLMNB1 expression were evaluated by qRT-PCR and...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691939/ https://www.ncbi.nlm.nih.gov/pubmed/31496737 http://dx.doi.org/10.2147/OTT.S204741 |
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author | He, Chunping Huang, Chao Zhou, Rui Yu, Honggang |
author_facet | He, Chunping Huang, Chao Zhou, Rui Yu, Honggang |
author_sort | He, Chunping |
collection | PubMed |
description | OBJECTIVE: The aberrant expression of circular RNAs (circRNAs) is a frequent occurrence in various cancers. However, the functions and roles played by most circRNAs in colorectal cancer (CRC) remain largely unknown. MATERIALS AND METHODS: Levels of circLMNB1 expression were evaluated by qRT-PCR and FISH assays. The influence of circLMNB1 knockdown on LoVo and HCT116 cell proliferation, cycling, apoptosis, migration, and invasion were assessed by the CCK-8, assay, Edu assay, flow cytometry, Hoechst staining, and the Transwell assay, respectively. The relative levels of EMT- and apoptosis-related proteins were determined by Western blotting. RESULTS: CircLMNB1 expression was significantly upregulated in CRC tissues and cells. Knockdown of circLMNB1 by siRNA in LoVo cells suppressed cell proliferation, migration and invasion, and facilitated cell cycle arrest and apoptosis In addition, we proved that knockdown of circLMNB1 upregulated E-cadherin, Bax and caspase-3 expression, and downregulated MMP2, MMP-9, and N-cadherin expression in LoVo cells. Further results showed that overexpression of circLMNB1 enhanced the malignant characteristics of HCT116 cells. CONCLUSION: Our findings revealed that blocking of circLMNB1 could inhibit CRC development, and help to explain the underlying mechanism by which circLMNB1 knockdown inhibits the metastasis of CRC. Finally, this study suggests circLMNB1 as a novel biomarker for CRC. |
format | Online Article Text |
id | pubmed-6691939 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-66919392019-09-06 CircLMNB1 promotes colorectal cancer by regulating cell proliferation, apoptosis and epithelial-mesenchymal transition He, Chunping Huang, Chao Zhou, Rui Yu, Honggang Onco Targets Ther Original Research OBJECTIVE: The aberrant expression of circular RNAs (circRNAs) is a frequent occurrence in various cancers. However, the functions and roles played by most circRNAs in colorectal cancer (CRC) remain largely unknown. MATERIALS AND METHODS: Levels of circLMNB1 expression were evaluated by qRT-PCR and FISH assays. The influence of circLMNB1 knockdown on LoVo and HCT116 cell proliferation, cycling, apoptosis, migration, and invasion were assessed by the CCK-8, assay, Edu assay, flow cytometry, Hoechst staining, and the Transwell assay, respectively. The relative levels of EMT- and apoptosis-related proteins were determined by Western blotting. RESULTS: CircLMNB1 expression was significantly upregulated in CRC tissues and cells. Knockdown of circLMNB1 by siRNA in LoVo cells suppressed cell proliferation, migration and invasion, and facilitated cell cycle arrest and apoptosis In addition, we proved that knockdown of circLMNB1 upregulated E-cadherin, Bax and caspase-3 expression, and downregulated MMP2, MMP-9, and N-cadherin expression in LoVo cells. Further results showed that overexpression of circLMNB1 enhanced the malignant characteristics of HCT116 cells. CONCLUSION: Our findings revealed that blocking of circLMNB1 could inhibit CRC development, and help to explain the underlying mechanism by which circLMNB1 knockdown inhibits the metastasis of CRC. Finally, this study suggests circLMNB1 as a novel biomarker for CRC. Dove 2019-08-09 /pmc/articles/PMC6691939/ /pubmed/31496737 http://dx.doi.org/10.2147/OTT.S204741 Text en © 2019 He et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research He, Chunping Huang, Chao Zhou, Rui Yu, Honggang CircLMNB1 promotes colorectal cancer by regulating cell proliferation, apoptosis and epithelial-mesenchymal transition |
title | CircLMNB1 promotes colorectal cancer by regulating cell proliferation, apoptosis and epithelial-mesenchymal transition |
title_full | CircLMNB1 promotes colorectal cancer by regulating cell proliferation, apoptosis and epithelial-mesenchymal transition |
title_fullStr | CircLMNB1 promotes colorectal cancer by regulating cell proliferation, apoptosis and epithelial-mesenchymal transition |
title_full_unstemmed | CircLMNB1 promotes colorectal cancer by regulating cell proliferation, apoptosis and epithelial-mesenchymal transition |
title_short | CircLMNB1 promotes colorectal cancer by regulating cell proliferation, apoptosis and epithelial-mesenchymal transition |
title_sort | circlmnb1 promotes colorectal cancer by regulating cell proliferation, apoptosis and epithelial-mesenchymal transition |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691939/ https://www.ncbi.nlm.nih.gov/pubmed/31496737 http://dx.doi.org/10.2147/OTT.S204741 |
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