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LINC00511 enhances LUAD malignancy by upregulating GCNT3 via miR-195-5p
BACKGROUND: Accumulating evidence suggests that LINC00511 acts as an oncogenic long non-coding RNA (lncRNA) in various cancers, including lung adenocarcinoma (LUAD). Hence, we attempted to elucidate the potential role of LINC00511 in LUAD. METHODS: LINC00511, miR-195-5p, and GCNT3 expression in LUAD...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8994914/ https://www.ncbi.nlm.nih.gov/pubmed/35399076 http://dx.doi.org/10.1186/s12885-022-09459-7 |
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author | Zhang, Youyi Xiao, Ping Hu, Xiaobo |
author_facet | Zhang, Youyi Xiao, Ping Hu, Xiaobo |
author_sort | Zhang, Youyi |
collection | PubMed |
description | BACKGROUND: Accumulating evidence suggests that LINC00511 acts as an oncogenic long non-coding RNA (lncRNA) in various cancers, including lung adenocarcinoma (LUAD). Hence, we attempted to elucidate the potential role of LINC00511 in LUAD. METHODS: LINC00511, miR-195-5p, and GCNT3 expression in LUAD was detected by qRT-PCR. Changes in the proliferation, migration, and invasion of LUAD cells after abnormal regulation of LINC00511, miR-195-5p, or GCNT3 were detected by CCK-8, BrdU, wound healing, and transwell assays. Bax and Bcl-2 protein expression was measured by western blotting. Additionally, we identified the targeting effects of LINC00511, miR-195-5p, and GCNT3 using luciferase and RNA immunoprecipitation (RIP) assays. RESULTS: LINC00511 and GCNT3 were found to be upregulated in LUAD, while miR-195-5p was downregulated. Silencing LINC00511 or GCNT3 decreased the proliferation, migration, invasion, and Bcl-2 protein content in LUAD cells and increased the expression of Bax. Interference with miR-195-5p promoted malignant proliferation of cancer cells. miR-195-5p expression was affected by LINC00511and targeted GCNT3. CONCLUSION: Silencing LINC00511 promotes GCNT3 expression by inhibiting miR-195-5p and ultimately stimulates the malignant progression of LUAD. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-022-09459-7. |
format | Online Article Text |
id | pubmed-8994914 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-89949142022-04-11 LINC00511 enhances LUAD malignancy by upregulating GCNT3 via miR-195-5p Zhang, Youyi Xiao, Ping Hu, Xiaobo BMC Cancer Research BACKGROUND: Accumulating evidence suggests that LINC00511 acts as an oncogenic long non-coding RNA (lncRNA) in various cancers, including lung adenocarcinoma (LUAD). Hence, we attempted to elucidate the potential role of LINC00511 in LUAD. METHODS: LINC00511, miR-195-5p, and GCNT3 expression in LUAD was detected by qRT-PCR. Changes in the proliferation, migration, and invasion of LUAD cells after abnormal regulation of LINC00511, miR-195-5p, or GCNT3 were detected by CCK-8, BrdU, wound healing, and transwell assays. Bax and Bcl-2 protein expression was measured by western blotting. Additionally, we identified the targeting effects of LINC00511, miR-195-5p, and GCNT3 using luciferase and RNA immunoprecipitation (RIP) assays. RESULTS: LINC00511 and GCNT3 were found to be upregulated in LUAD, while miR-195-5p was downregulated. Silencing LINC00511 or GCNT3 decreased the proliferation, migration, invasion, and Bcl-2 protein content in LUAD cells and increased the expression of Bax. Interference with miR-195-5p promoted malignant proliferation of cancer cells. miR-195-5p expression was affected by LINC00511and targeted GCNT3. CONCLUSION: Silencing LINC00511 promotes GCNT3 expression by inhibiting miR-195-5p and ultimately stimulates the malignant progression of LUAD. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-022-09459-7. BioMed Central 2022-04-10 /pmc/articles/PMC8994914/ /pubmed/35399076 http://dx.doi.org/10.1186/s12885-022-09459-7 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Zhang, Youyi Xiao, Ping Hu, Xiaobo LINC00511 enhances LUAD malignancy by upregulating GCNT3 via miR-195-5p |
title | LINC00511 enhances LUAD malignancy by upregulating GCNT3 via miR-195-5p |
title_full | LINC00511 enhances LUAD malignancy by upregulating GCNT3 via miR-195-5p |
title_fullStr | LINC00511 enhances LUAD malignancy by upregulating GCNT3 via miR-195-5p |
title_full_unstemmed | LINC00511 enhances LUAD malignancy by upregulating GCNT3 via miR-195-5p |
title_short | LINC00511 enhances LUAD malignancy by upregulating GCNT3 via miR-195-5p |
title_sort | linc00511 enhances luad malignancy by upregulating gcnt3 via mir-195-5p |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8994914/ https://www.ncbi.nlm.nih.gov/pubmed/35399076 http://dx.doi.org/10.1186/s12885-022-09459-7 |
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