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lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression: ELFN1-AS1 promotes gastric cancer progression
Long noncoding RNA (lncRNA) extracellular leucine rich repeat and fibronectin type III domain containing 1-antisense RNA 1 (ELFN1-AS1) has been found to be upregulated in various tumors. However, the biological functions of ELFN1-AS1 in gastric cancer (GC) are not entirely understood. In the present...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10160233/ https://www.ncbi.nlm.nih.gov/pubmed/36876422 http://dx.doi.org/10.3724/abbs.2023023 |
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author | Huang, Jinxi Yuan, Weiwei Chen, Beibei Li, Gaofeng Chen, Xiaobing |
author_facet | Huang, Jinxi Yuan, Weiwei Chen, Beibei Li, Gaofeng Chen, Xiaobing |
author_sort | Huang, Jinxi |
collection | PubMed |
description | Long noncoding RNA (lncRNA) extracellular leucine rich repeat and fibronectin type III domain containing 1-antisense RNA 1 (ELFN1-AS1) has been found to be upregulated in various tumors. However, the biological functions of ELFN1-AS1 in gastric cancer (GC) are not entirely understood. In the present study, the expression levels of ELFN1-AS1, miR-211-3p, and TRIM29 are determined using reverse transcription-quantitative PCR. Subsequently, CCK8, EdU, and colony formation assays are performed to determine GC cell vitality. The migratory and invasive capabilities of GC cells are further evaluated using transwell invasion and cell scratch assays. Western blot analysis is performed to quantify the levels of proteins associated with GC cell apoptosis and epithelialmesenchymal transition (EMT). The competing endogenous RNA (ceRNA) activity of ELFN1-AS1 on TRIM29 through miR-211-3p is confirmed by pull-down, RIP, and luciferase reporter assays. Our study proves that ELFN1-AS1 and TRIM29 are highly expressed in GC tissues. ELFN1-AS1 silencing inhibits GC cell proliferation, migration, invasion and EMT, and induces cell apoptosis. Rescue experiments reveal that the oncogenicity of ELFN1-AS1 is modulated by acting as a sponge for miR-211-3p, thereby increasing the expression of the target gene of miR-211-3p, TRIM29. In summary, ELFN1-AS1 maintains GC cell tumorigenicity via the ELFN1-AS1/miR-211-3p/TRIM29 axis, indicating that this axis can be directed for GC treatment in the future. |
format | Online Article Text |
id | pubmed-10160233 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-101602332023-05-06 lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression: ELFN1-AS1 promotes gastric cancer progression Huang, Jinxi Yuan, Weiwei Chen, Beibei Li, Gaofeng Chen, Xiaobing Acta Biochim Biophys Sin (Shanghai) Research Article Long noncoding RNA (lncRNA) extracellular leucine rich repeat and fibronectin type III domain containing 1-antisense RNA 1 (ELFN1-AS1) has been found to be upregulated in various tumors. However, the biological functions of ELFN1-AS1 in gastric cancer (GC) are not entirely understood. In the present study, the expression levels of ELFN1-AS1, miR-211-3p, and TRIM29 are determined using reverse transcription-quantitative PCR. Subsequently, CCK8, EdU, and colony formation assays are performed to determine GC cell vitality. The migratory and invasive capabilities of GC cells are further evaluated using transwell invasion and cell scratch assays. Western blot analysis is performed to quantify the levels of proteins associated with GC cell apoptosis and epithelialmesenchymal transition (EMT). The competing endogenous RNA (ceRNA) activity of ELFN1-AS1 on TRIM29 through miR-211-3p is confirmed by pull-down, RIP, and luciferase reporter assays. Our study proves that ELFN1-AS1 and TRIM29 are highly expressed in GC tissues. ELFN1-AS1 silencing inhibits GC cell proliferation, migration, invasion and EMT, and induces cell apoptosis. Rescue experiments reveal that the oncogenicity of ELFN1-AS1 is modulated by acting as a sponge for miR-211-3p, thereby increasing the expression of the target gene of miR-211-3p, TRIM29. In summary, ELFN1-AS1 maintains GC cell tumorigenicity via the ELFN1-AS1/miR-211-3p/TRIM29 axis, indicating that this axis can be directed for GC treatment in the future. Oxford University Press 2023-03-03 /pmc/articles/PMC10160233/ /pubmed/36876422 http://dx.doi.org/10.3724/abbs.2023023 Text en © The Author(s) 2021. 0 https://creativecommons.org/licenses/by-nc/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/). |
spellingShingle | Research Article Huang, Jinxi Yuan, Weiwei Chen, Beibei Li, Gaofeng Chen, Xiaobing lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression: ELFN1-AS1 promotes gastric cancer progression |
title | lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression: ELFN1-AS1 promotes gastric cancer progression |
title_full | lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression: ELFN1-AS1 promotes gastric cancer progression |
title_fullStr | lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression: ELFN1-AS1 promotes gastric cancer progression |
title_full_unstemmed | lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression: ELFN1-AS1 promotes gastric cancer progression |
title_short | lncRNA ELFN1-AS1 upregulates TRIM29 by suppressing miR-211-3p to promote gastric cancer progression: ELFN1-AS1 promotes gastric cancer progression |
title_sort | lncrna elfn1-as1 upregulates trim29 by suppressing mir-211-3p to promote gastric cancer progression: elfn1-as1 promotes gastric cancer progression |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10160233/ https://www.ncbi.nlm.nih.gov/pubmed/36876422 http://dx.doi.org/10.3724/abbs.2023023 |
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