Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: E, Zhang, Li, Chunli, Xiang, Yuandi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: De Gruyter 2020
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
_version_ 1783619531954978816
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
work_keys_str_mv AT ezhang lncrnafoxd3as1mir135a5pfunctioninnasopharyngealcarcinomacells
AT lichunli lncrnafoxd3as1mir135a5pfunctioninnasopharyngealcarcinomacells
AT xiangyuandi lncrnafoxd3as1mir135a5pfunctioninnasopharyngealcarcinomacells