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Eicosapentaenoic acid’s metabolism of 15-LOX-1 promotes the expression of miR-101 thus inhibits Cox2 pathway in colon cancer
PURPOSE: It is well known that diet Eicosapentaenoic acid (EPA) is beneficial to colon cancer (CC). However, the underlying molecular mechanisms of EPA-relating miRNAs on genesis and development of this area is still unclear. MATERIALS AND METHODS: This study tries to find the function and specific...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305347/ https://www.ncbi.nlm.nih.gov/pubmed/32606775 http://dx.doi.org/10.2147/OTT.S237562 |
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author | Cai, Yi Liu, Jie Cai, Shao-kang Miao, Er-ya Jia, Cheng-qian Fan, Yong-zhi Li, Ying-bo |
author_facet | Cai, Yi Liu, Jie Cai, Shao-kang Miao, Er-ya Jia, Cheng-qian Fan, Yong-zhi Li, Ying-bo |
author_sort | Cai, Yi |
collection | PubMed |
description | PURPOSE: It is well known that diet Eicosapentaenoic acid (EPA) is beneficial to colon cancer (CC). However, the underlying molecular mechanisms of EPA-relating miRNAs on genesis and development of this area is still unclear. MATERIALS AND METHODS: This study tries to find the function and specific role of EPA in CC through quantitative PCR (qPCR), Western blotting, immunofluorescence (IF), mass spectrometry, and immunohistochemistry (IHC) assays. By these methods, the enrichment of 15-LOX-1 metabolites of EPA, the expression of miR-101 and Cox2, and the relationship among them in CC are measured. RESULTS: The quantity of miR-101 was obviously suppressed in CC tissues and SW480 cells. After application of miR-101 mimics in CC cell lines, the Cox2 expression was inhibited too. Next, we confirmed that EPA could increase the expression of miR-101 induced by 15-LOX-1. Finally, we tested whether EPA functions as a regulator of miR-101 via the production of resolvin E3. CONCLUSION: Our data demonstrate that the EPA–15-LOX-1–miR-101-Cox2 signaling pathway owns a crucial position in the pathogenesis and development of diet-related CC. These findings exert exciting meanings for presenting new therapeutic angles in CC. |
format | Online Article Text |
id | pubmed-7305347 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-73053472020-06-29 Eicosapentaenoic acid’s metabolism of 15-LOX-1 promotes the expression of miR-101 thus inhibits Cox2 pathway in colon cancer Cai, Yi Liu, Jie Cai, Shao-kang Miao, Er-ya Jia, Cheng-qian Fan, Yong-zhi Li, Ying-bo Onco Targets Ther Original Research PURPOSE: It is well known that diet Eicosapentaenoic acid (EPA) is beneficial to colon cancer (CC). However, the underlying molecular mechanisms of EPA-relating miRNAs on genesis and development of this area is still unclear. MATERIALS AND METHODS: This study tries to find the function and specific role of EPA in CC through quantitative PCR (qPCR), Western blotting, immunofluorescence (IF), mass spectrometry, and immunohistochemistry (IHC) assays. By these methods, the enrichment of 15-LOX-1 metabolites of EPA, the expression of miR-101 and Cox2, and the relationship among them in CC are measured. RESULTS: The quantity of miR-101 was obviously suppressed in CC tissues and SW480 cells. After application of miR-101 mimics in CC cell lines, the Cox2 expression was inhibited too. Next, we confirmed that EPA could increase the expression of miR-101 induced by 15-LOX-1. Finally, we tested whether EPA functions as a regulator of miR-101 via the production of resolvin E3. CONCLUSION: Our data demonstrate that the EPA–15-LOX-1–miR-101-Cox2 signaling pathway owns a crucial position in the pathogenesis and development of diet-related CC. These findings exert exciting meanings for presenting new therapeutic angles in CC. Dove 2020-06-15 /pmc/articles/PMC7305347/ /pubmed/32606775 http://dx.doi.org/10.2147/OTT.S237562 Text en © 2020 Cai 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 Cai, Yi Liu, Jie Cai, Shao-kang Miao, Er-ya Jia, Cheng-qian Fan, Yong-zhi Li, Ying-bo Eicosapentaenoic acid’s metabolism of 15-LOX-1 promotes the expression of miR-101 thus inhibits Cox2 pathway in colon cancer |
title | Eicosapentaenoic acid’s metabolism of 15-LOX-1 promotes the expression of miR-101 thus inhibits Cox2 pathway in colon cancer |
title_full | Eicosapentaenoic acid’s metabolism of 15-LOX-1 promotes the expression of miR-101 thus inhibits Cox2 pathway in colon cancer |
title_fullStr | Eicosapentaenoic acid’s metabolism of 15-LOX-1 promotes the expression of miR-101 thus inhibits Cox2 pathway in colon cancer |
title_full_unstemmed | Eicosapentaenoic acid’s metabolism of 15-LOX-1 promotes the expression of miR-101 thus inhibits Cox2 pathway in colon cancer |
title_short | Eicosapentaenoic acid’s metabolism of 15-LOX-1 promotes the expression of miR-101 thus inhibits Cox2 pathway in colon cancer |
title_sort | eicosapentaenoic acid’s metabolism of 15-lox-1 promotes the expression of mir-101 thus inhibits cox2 pathway in colon cancer |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305347/ https://www.ncbi.nlm.nih.gov/pubmed/32606775 http://dx.doi.org/10.2147/OTT.S237562 |
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