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Sevoflurane Suppresses Colon Cancer Cell Malignancy by Regulating circ-PI4KA

PURPOSE: To explore the effect of SEV on colon cancer cells through circ-PI4KA. METHODS: The RNA level of circular RNA_0062389, microRNA-331-3p and LIM and SH3 protein 1 was determined by quantitative real-time polymerase chain reaction. Protein expression was detected by Western blot. Cell prolifer...

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Autores principales: Sun, Suqing, Wang, Peng, Ren, Lijie, Wang, Hongli, Zhan, Yanli, Shan, Shimin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8144176/
https://www.ncbi.nlm.nih.gov/pubmed/34045869
http://dx.doi.org/10.2147/OTT.S295552
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author Sun, Suqing
Wang, Peng
Ren, Lijie
Wang, Hongli
Zhan, Yanli
Shan, Shimin
author_facet Sun, Suqing
Wang, Peng
Ren, Lijie
Wang, Hongli
Zhan, Yanli
Shan, Shimin
author_sort Sun, Suqing
collection PubMed
description PURPOSE: To explore the effect of SEV on colon cancer cells through circ-PI4KA. METHODS: The RNA level of circular RNA_0062389, microRNA-331-3p and LIM and SH3 protein 1 was determined by quantitative real-time polymerase chain reaction. Protein expression was detected by Western blot. Cell proliferation was investigated by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide, cell colony formation and 5-ethynyl-29-deoxyuridine assays. Cell apoptosis was demonstrated using Annexin V-fluorescein isothiocyanate/propidium iodide double staining assay. Cell migration and invasion were detected by transwell assay. The target relationship between miR-331-3p and circ-PI4KA or LASP1 was predicted by starBase v2.0 online database, and identified by a dual-luciferase reporter assay. The effects between SEV treatment and circ-PI4KA knockdown on tumor formation were presented by in vivo tumor formation assay. RESULTS: Circ-PI4KA and LASP1 expressions were dramatically upregulated, while miR-331-3p was downregulated in colon cancer tissues and cells, respectively. SEV exposure significantly decreased the expression of circ-PI4KA and LASP1, but increased miR-331-3p expression. SEV inhibited cell proliferation, migration and invasion, and induced cell apoptosis by regulating circ-PI4KA. Furthermore, circ-PI4KA interacted with miR-331-3p, and miR-331-3p interacted with LASP1. SEV inhibited tumor growth by controlling circ-PI4KA in vivo. CONCLUSION: Circ-PI4KA attenuated SEV-treated colon cancer cell malignancy by upregulating LASP1 through binding to miR-331-3p, which provided a new mechanism for studying surgery-mediated therapy of colon cancer.
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spelling pubmed-81441762021-05-26 Sevoflurane Suppresses Colon Cancer Cell Malignancy by Regulating circ-PI4KA Sun, Suqing Wang, Peng Ren, Lijie Wang, Hongli Zhan, Yanli Shan, Shimin Onco Targets Ther Original Research PURPOSE: To explore the effect of SEV on colon cancer cells through circ-PI4KA. METHODS: The RNA level of circular RNA_0062389, microRNA-331-3p and LIM and SH3 protein 1 was determined by quantitative real-time polymerase chain reaction. Protein expression was detected by Western blot. Cell proliferation was investigated by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide, cell colony formation and 5-ethynyl-29-deoxyuridine assays. Cell apoptosis was demonstrated using Annexin V-fluorescein isothiocyanate/propidium iodide double staining assay. Cell migration and invasion were detected by transwell assay. The target relationship between miR-331-3p and circ-PI4KA or LASP1 was predicted by starBase v2.0 online database, and identified by a dual-luciferase reporter assay. The effects between SEV treatment and circ-PI4KA knockdown on tumor formation were presented by in vivo tumor formation assay. RESULTS: Circ-PI4KA and LASP1 expressions were dramatically upregulated, while miR-331-3p was downregulated in colon cancer tissues and cells, respectively. SEV exposure significantly decreased the expression of circ-PI4KA and LASP1, but increased miR-331-3p expression. SEV inhibited cell proliferation, migration and invasion, and induced cell apoptosis by regulating circ-PI4KA. Furthermore, circ-PI4KA interacted with miR-331-3p, and miR-331-3p interacted with LASP1. SEV inhibited tumor growth by controlling circ-PI4KA in vivo. CONCLUSION: Circ-PI4KA attenuated SEV-treated colon cancer cell malignancy by upregulating LASP1 through binding to miR-331-3p, which provided a new mechanism for studying surgery-mediated therapy of colon cancer. Dove 2021-05-20 /pmc/articles/PMC8144176/ /pubmed/34045869 http://dx.doi.org/10.2147/OTT.S295552 Text en © 2021 Sun et al. https://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/ (https://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
Sun, Suqing
Wang, Peng
Ren, Lijie
Wang, Hongli
Zhan, Yanli
Shan, Shimin
Sevoflurane Suppresses Colon Cancer Cell Malignancy by Regulating circ-PI4KA
title Sevoflurane Suppresses Colon Cancer Cell Malignancy by Regulating circ-PI4KA
title_full Sevoflurane Suppresses Colon Cancer Cell Malignancy by Regulating circ-PI4KA
title_fullStr Sevoflurane Suppresses Colon Cancer Cell Malignancy by Regulating circ-PI4KA
title_full_unstemmed Sevoflurane Suppresses Colon Cancer Cell Malignancy by Regulating circ-PI4KA
title_short Sevoflurane Suppresses Colon Cancer Cell Malignancy by Regulating circ-PI4KA
title_sort sevoflurane suppresses colon cancer cell malignancy by regulating circ-pi4ka
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8144176/
https://www.ncbi.nlm.nih.gov/pubmed/34045869
http://dx.doi.org/10.2147/OTT.S295552
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