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Apolipoprotein C1 (APOC1) promotes tumor progression via MAPK signaling pathways in colorectal cancer
Aim: Identifying high-efficiency prognostic markers for colorectal cancer (CRC) is necessary for clinical practice. Increasing evidence demonstrates that apolipoprotein C1 (APOC1) promotes carcinogenesis in some human cancers. However, the expression status and biological function of APOC1 in CRC re...
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/PMC6549782/ https://www.ncbi.nlm.nih.gov/pubmed/31213910 http://dx.doi.org/10.2147/CMAR.S192529 |
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author | Ren, Hui Chen, Zhihui Yang, Liang Xiong, Weixin Yang, Hong Xu, Kaiwu Zhai, Ertao Ding, Li He, Yulong Song, Xingming |
author_facet | Ren, Hui Chen, Zhihui Yang, Liang Xiong, Weixin Yang, Hong Xu, Kaiwu Zhai, Ertao Ding, Li He, Yulong Song, Xingming |
author_sort | Ren, Hui |
collection | PubMed |
description | Aim: Identifying high-efficiency prognostic markers for colorectal cancer (CRC) is necessary for clinical practice. Increasing evidence demonstrates that apolipoprotein C1 (APOC1) promotes carcinogenesis in some human cancers. However, the expression status and biological function of APOC1 in CRC remain unclear. Materials and methods: We detected the association between APOC1 expression and clinicopathological features in 140 CRC patients by immunohistochemistry. Small interfering RNA (siRNA) technology was used to downregulate APOC1 expression in CRC cells. Cell proliferation was estimated by CCK8 and clonogenic assays. The cell cycle and apoptosis were analyzed by flow cytometry. Cell migration and invasion were examined by a transwell assay. Gene set enrichment analysis (GSEA) and protein expression of signaling pathways were used to suggest the possible APOC1-associated pathways in CRC. Results: APOC1 was highly expressed in CRC tissues. High immunohistochemistry (IHC) expression of APOC1 was correlated with the N stage, M stage and TNM stage. High IHC APOC1 expression in CRC tissues was associated with poor prognosis. Univariate and multivariate Cox regression analyses showed that APOC1 was an independent risk factor for OS. Cell proliferation of CRC cell lines was inhibited by the downregulation of APOC1. Moreover, si-APOC1 transfection induced cell cycle arrest but low apoptosis increases by regulating the expression of related proteins. Cell migration and invasion were also inhibited by the downregulation of APOC1. The Cancer Genome Atlas Colorectal Adenocarcinoma (TCGA COAD-READ) dataset analyzed by GSEA showed that APOC1 might be involved in the mitogen-activated protein kinase (MAPK) signaling pathway, which was further preliminarily confirmed by Western blotting. Conclusion: APOC1 was overexpressed in CRC tissues, and a high level of APOC1 contributed to a poor prognosis. APOC1 expression influenced the cell proliferation ability and motility capacity of CRC via the MAPK pathway. APOC1 could act as a novel prognostic biomarker in CRC. |
format | Online Article Text |
id | pubmed-6549782 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-65497822019-06-18 Apolipoprotein C1 (APOC1) promotes tumor progression via MAPK signaling pathways in colorectal cancer Ren, Hui Chen, Zhihui Yang, Liang Xiong, Weixin Yang, Hong Xu, Kaiwu Zhai, Ertao Ding, Li He, Yulong Song, Xingming Cancer Manag Res Original Research Aim: Identifying high-efficiency prognostic markers for colorectal cancer (CRC) is necessary for clinical practice. Increasing evidence demonstrates that apolipoprotein C1 (APOC1) promotes carcinogenesis in some human cancers. However, the expression status and biological function of APOC1 in CRC remain unclear. Materials and methods: We detected the association between APOC1 expression and clinicopathological features in 140 CRC patients by immunohistochemistry. Small interfering RNA (siRNA) technology was used to downregulate APOC1 expression in CRC cells. Cell proliferation was estimated by CCK8 and clonogenic assays. The cell cycle and apoptosis were analyzed by flow cytometry. Cell migration and invasion were examined by a transwell assay. Gene set enrichment analysis (GSEA) and protein expression of signaling pathways were used to suggest the possible APOC1-associated pathways in CRC. Results: APOC1 was highly expressed in CRC tissues. High immunohistochemistry (IHC) expression of APOC1 was correlated with the N stage, M stage and TNM stage. High IHC APOC1 expression in CRC tissues was associated with poor prognosis. Univariate and multivariate Cox regression analyses showed that APOC1 was an independent risk factor for OS. Cell proliferation of CRC cell lines was inhibited by the downregulation of APOC1. Moreover, si-APOC1 transfection induced cell cycle arrest but low apoptosis increases by regulating the expression of related proteins. Cell migration and invasion were also inhibited by the downregulation of APOC1. The Cancer Genome Atlas Colorectal Adenocarcinoma (TCGA COAD-READ) dataset analyzed by GSEA showed that APOC1 might be involved in the mitogen-activated protein kinase (MAPK) signaling pathway, which was further preliminarily confirmed by Western blotting. Conclusion: APOC1 was overexpressed in CRC tissues, and a high level of APOC1 contributed to a poor prognosis. APOC1 expression influenced the cell proliferation ability and motility capacity of CRC via the MAPK pathway. APOC1 could act as a novel prognostic biomarker in CRC. Dove 2019-05-29 /pmc/articles/PMC6549782/ /pubmed/31213910 http://dx.doi.org/10.2147/CMAR.S192529 Text en © 2019 Ren 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 Ren, Hui Chen, Zhihui Yang, Liang Xiong, Weixin Yang, Hong Xu, Kaiwu Zhai, Ertao Ding, Li He, Yulong Song, Xingming Apolipoprotein C1 (APOC1) promotes tumor progression via MAPK signaling pathways in colorectal cancer |
title | Apolipoprotein C1 (APOC1) promotes tumor progression via MAPK signaling pathways in colorectal cancer |
title_full | Apolipoprotein C1 (APOC1) promotes tumor progression via MAPK signaling pathways in colorectal cancer |
title_fullStr | Apolipoprotein C1 (APOC1) promotes tumor progression via MAPK signaling pathways in colorectal cancer |
title_full_unstemmed | Apolipoprotein C1 (APOC1) promotes tumor progression via MAPK signaling pathways in colorectal cancer |
title_short | Apolipoprotein C1 (APOC1) promotes tumor progression via MAPK signaling pathways in colorectal cancer |
title_sort | apolipoprotein c1 (apoc1) promotes tumor progression via mapk signaling pathways in colorectal cancer |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6549782/ https://www.ncbi.nlm.nih.gov/pubmed/31213910 http://dx.doi.org/10.2147/CMAR.S192529 |
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