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Small interfering RNA-mediated knockdown of KRT80 suppresses colorectal cancer proliferation
Colorectal cancer (CRC) is the third most common cancer in the world and its development is associated with oncogenic dysfunction. Therefore, the present study aimed to identify differentially expressed genes (DEGs) in CRC tissues and to determine the role of keratin 80 (KRT80) in CRC cell prolifera...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7579811/ https://www.ncbi.nlm.nih.gov/pubmed/33101466 http://dx.doi.org/10.3892/etm.2020.9306 |
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author | Lin, Jiatian Fan, Xiaoqin Chen, Junhui Xie, Xina Yu, Hongjian |
author_facet | Lin, Jiatian Fan, Xiaoqin Chen, Junhui Xie, Xina Yu, Hongjian |
author_sort | Lin, Jiatian |
collection | PubMed |
description | Colorectal cancer (CRC) is the third most common cancer in the world and its development is associated with oncogenic dysfunction. Therefore, the present study aimed to identify differentially expressed genes (DEGs) in CRC tissues and to determine the role of keratin 80 (KRT80) in CRC cell proliferation. DEGs were initially screened in 32 paired CRC tissues and matched adjacent normal tissues from RNA-Seq datasets in The Cancer Genome Atlas database using the limma package in R software. In total, 2,114 DEGs were identified, of which KRT80 was discovered to be the most upregulated in CRC tissues. Moreover, increased KRT80 expression levels were confirmed in tissues collected from 50 patients with CRC using reverse transcription-quantitative PCR, and its increased expression levels were significantly associated with increased lymph node and distant metastasis and a higher pathological stage. Furthermore, KRT80 knockdown using siRNA decreased the viability and proliferation of CRC cells. Finally, pathway analysis revealed that the proteins co-expressed with KRT80 in CRC were enriched in the cell cycle, DNA replication, immune system, metabolism of protein and RNA, signal transduction and other cellular processes. Among them, the cell cycle and DNA replication pathways contained the highest number of the proteins identified. In conclusion, the findings of the present study suggested that KRT80 may be overexpressed in CRC tissues. Furthermore, KRT80 may be involved in the proliferation of CRC cells, which is likely through its ability to regulate the cell cycle and DNA replication pathways, thus it may serve as a potential therapeutic target for patients with CRC. |
format | Online Article Text |
id | pubmed-7579811 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-75798112020-10-22 Small interfering RNA-mediated knockdown of KRT80 suppresses colorectal cancer proliferation Lin, Jiatian Fan, Xiaoqin Chen, Junhui Xie, Xina Yu, Hongjian Exp Ther Med Articles Colorectal cancer (CRC) is the third most common cancer in the world and its development is associated with oncogenic dysfunction. Therefore, the present study aimed to identify differentially expressed genes (DEGs) in CRC tissues and to determine the role of keratin 80 (KRT80) in CRC cell proliferation. DEGs were initially screened in 32 paired CRC tissues and matched adjacent normal tissues from RNA-Seq datasets in The Cancer Genome Atlas database using the limma package in R software. In total, 2,114 DEGs were identified, of which KRT80 was discovered to be the most upregulated in CRC tissues. Moreover, increased KRT80 expression levels were confirmed in tissues collected from 50 patients with CRC using reverse transcription-quantitative PCR, and its increased expression levels were significantly associated with increased lymph node and distant metastasis and a higher pathological stage. Furthermore, KRT80 knockdown using siRNA decreased the viability and proliferation of CRC cells. Finally, pathway analysis revealed that the proteins co-expressed with KRT80 in CRC were enriched in the cell cycle, DNA replication, immune system, metabolism of protein and RNA, signal transduction and other cellular processes. Among them, the cell cycle and DNA replication pathways contained the highest number of the proteins identified. In conclusion, the findings of the present study suggested that KRT80 may be overexpressed in CRC tissues. Furthermore, KRT80 may be involved in the proliferation of CRC cells, which is likely through its ability to regulate the cell cycle and DNA replication pathways, thus it may serve as a potential therapeutic target for patients with CRC. D.A. Spandidos 2020-12 2020-10-09 /pmc/articles/PMC7579811/ /pubmed/33101466 http://dx.doi.org/10.3892/etm.2020.9306 Text en Copyright: © Lin 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 Lin, Jiatian Fan, Xiaoqin Chen, Junhui Xie, Xina Yu, Hongjian Small interfering RNA-mediated knockdown of KRT80 suppresses colorectal cancer proliferation |
title | Small interfering RNA-mediated knockdown of KRT80 suppresses colorectal cancer proliferation |
title_full | Small interfering RNA-mediated knockdown of KRT80 suppresses colorectal cancer proliferation |
title_fullStr | Small interfering RNA-mediated knockdown of KRT80 suppresses colorectal cancer proliferation |
title_full_unstemmed | Small interfering RNA-mediated knockdown of KRT80 suppresses colorectal cancer proliferation |
title_short | Small interfering RNA-mediated knockdown of KRT80 suppresses colorectal cancer proliferation |
title_sort | small interfering rna-mediated knockdown of krt80 suppresses colorectal cancer proliferation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7579811/ https://www.ncbi.nlm.nih.gov/pubmed/33101466 http://dx.doi.org/10.3892/etm.2020.9306 |
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