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LncRNA FOXD3-AS1/miR-135a-5p function in nasopharyngeal carcinoma cells
This research aimed to illustrate the biological function and associated regulatory mechanism of lncRNA FOXD3-AS1 (FOXD3-AS1) in nasopharyngeal carcinoma (NPC). This research initially found that FOXD3-AS1 was obviously upregulated in NPC cell lines by quantitative reverse transcription polymerase c...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
De Gruyter
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7718651/ https://www.ncbi.nlm.nih.gov/pubmed/33336076 http://dx.doi.org/10.1515/med-2020-0177 |
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author | E, Zhang Li, Chunli Xiang, Yuandi |
author_facet | E, Zhang Li, Chunli Xiang, Yuandi |
author_sort | E, Zhang |
collection | PubMed |
description | This research aimed to illustrate the biological function and associated regulatory mechanism of lncRNA FOXD3-AS1 (FOXD3-AS1) in nasopharyngeal carcinoma (NPC). This research initially found that FOXD3-AS1 was obviously upregulated in NPC cell lines by quantitative reverse transcription polymerase chain reaction (qRT-PCR) detection. Next, the direct target of FOXD3-AS1 was predicted by bioinformatics and further verified by dual-luciferase reporter assay. MiroRNA-135a-5p (miR-135a-5p) was identified as the target gene of FOXD3-AS1 and down-expressed in C666-1 cells compared to NP69. In addition, function assays were conducted in C666-1 cells, including methyl tetrazolium assay, flow cytometry, Caspase3 activity detection, and western blot assay. Our results suggested that miR-135a-5p upregulation inhibited NPC cell growth, enhanced cell apoptosis, promoted Caspase3 activity, increased cleaved-Caspase3, and reduced pro-Caspase3 level. Moreover, we found that FOXD3-AS1 knockdown notably inhibited C666-1 cell proliferation, increased cell apoptosis, enhanced Caspase3 activity, enhanced cleaved-Caspase3 expression, and suppressed pro-Caspase3 level in C666-1 cells. However, these findings were reversed in C666-1 cells by miR-135a-5p mimic co-transfection. To sum up, our data showed that FOXD3-AS1 knockdown regulated cell growth and apoptosis in NCP cells via altering miR-135a-5p expression, suggesting that FOXD3-AS1 might be a therapeutic target for NPC diagnosis and treatment. |
format | Online Article Text |
id | pubmed-7718651 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | De Gruyter |
record_format | MEDLINE/PubMed |
spelling | pubmed-77186512020-12-16 LncRNA FOXD3-AS1/miR-135a-5p function in nasopharyngeal carcinoma cells E, Zhang Li, Chunli Xiang, Yuandi Open Med (Wars) Research Article This research aimed to illustrate the biological function and associated regulatory mechanism of lncRNA FOXD3-AS1 (FOXD3-AS1) in nasopharyngeal carcinoma (NPC). This research initially found that FOXD3-AS1 was obviously upregulated in NPC cell lines by quantitative reverse transcription polymerase chain reaction (qRT-PCR) detection. Next, the direct target of FOXD3-AS1 was predicted by bioinformatics and further verified by dual-luciferase reporter assay. MiroRNA-135a-5p (miR-135a-5p) was identified as the target gene of FOXD3-AS1 and down-expressed in C666-1 cells compared to NP69. In addition, function assays were conducted in C666-1 cells, including methyl tetrazolium assay, flow cytometry, Caspase3 activity detection, and western blot assay. Our results suggested that miR-135a-5p upregulation inhibited NPC cell growth, enhanced cell apoptosis, promoted Caspase3 activity, increased cleaved-Caspase3, and reduced pro-Caspase3 level. Moreover, we found that FOXD3-AS1 knockdown notably inhibited C666-1 cell proliferation, increased cell apoptosis, enhanced Caspase3 activity, enhanced cleaved-Caspase3 expression, and suppressed pro-Caspase3 level in C666-1 cells. However, these findings were reversed in C666-1 cells by miR-135a-5p mimic co-transfection. To sum up, our data showed that FOXD3-AS1 knockdown regulated cell growth and apoptosis in NCP cells via altering miR-135a-5p expression, suggesting that FOXD3-AS1 might be a therapeutic target for NPC diagnosis and treatment. De Gruyter 2020-11-28 /pmc/articles/PMC7718651/ /pubmed/33336076 http://dx.doi.org/10.1515/med-2020-0177 Text en © 2020 Zhang E et al., published by De Gruyter http://creativecommons.org/licenses/by/4.0 This work is licensed under the Creative Commons Attribution 4.0 International License. |
spellingShingle | Research Article E, Zhang Li, Chunli Xiang, Yuandi LncRNA FOXD3-AS1/miR-135a-5p function in nasopharyngeal carcinoma cells |
title | LncRNA FOXD3-AS1/miR-135a-5p function in nasopharyngeal carcinoma cells |
title_full | LncRNA FOXD3-AS1/miR-135a-5p function in nasopharyngeal carcinoma cells |
title_fullStr | LncRNA FOXD3-AS1/miR-135a-5p function in nasopharyngeal carcinoma cells |
title_full_unstemmed | LncRNA FOXD3-AS1/miR-135a-5p function in nasopharyngeal carcinoma cells |
title_short | LncRNA FOXD3-AS1/miR-135a-5p function in nasopharyngeal carcinoma cells |
title_sort | lncrna foxd3-as1/mir-135a-5p function in nasopharyngeal carcinoma cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7718651/ https://www.ncbi.nlm.nih.gov/pubmed/33336076 http://dx.doi.org/10.1515/med-2020-0177 |
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