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LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1

Nasopharyngeal carcinoma (NPC) is a malignant tumor caused by nasopharyngeal epithelium. Long non-coding RNAs (lncRNAs) and microRNAs have been identified as vital regulators in many tumors, including NPC. This study aimed to explain the biological roles and relevant mechanisms of lncRNA FOXP4-AS1 (...

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Autores principales: Yan, Jin, Zhou, Qi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10569675/
https://www.ncbi.nlm.nih.gov/pubmed/36961080
http://dx.doi.org/10.1097/CAD.0000000000001510
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author Yan, Jin
Zhou, Qi
author_facet Yan, Jin
Zhou, Qi
author_sort Yan, Jin
collection PubMed
description Nasopharyngeal carcinoma (NPC) is a malignant tumor caused by nasopharyngeal epithelium. Long non-coding RNAs (lncRNAs) and microRNAs have been identified as vital regulators in many tumors, including NPC. This study aimed to explain the biological roles and relevant mechanisms of lncRNA FOXP4-AS1 (FOXP4-AS1) in NPC. The levels of lncRNA FOXP4-AS1, miR-136-5p and MAPK1 in C666-1 and NP69 cells were analyzed by quantitative reverse transcription PCR (qRT-PCR). C666-1 cells viability, migration and invasion were evaluated by MTT and Transwell assay, respectively. The target gene of miR-136-5p predicted by TargetScan was further verified using dual luciferase reporter assay. Moreover, qRT-PCR and Western blot were adopted to assess epithelial–mesenchymal transition (EMT)-related gene expression, including E-cadherin and N-cadherin. We found that lncRNA FOXP4-AS1 was upregulated, while miR-136-5p was low-expressed in C666-1 cells, as opposed to NP69. Knockdown of FOXP4-AS1 notably suppressed C666-1 cell growth, inhibited cell migration and invasion. We also observed that E-cadherin expression was fortified and N-cadherin level was decreased in C666-1 cells after FOXP4-AS1-siRNA transfection. However, all these findings were eliminated in C666-1 cells after miR-136-5p inhibitor treatment. We also found miR-136-5p directly targeted MAPK1 and correlated inversely with MAPK1 expression in C666-1 cells. Further investigation suggested that MAPK1-plasmid reversed the effects of miR-136-5p mimic on cells viability, migration, invasion and EMT. To conclude, our data revealed that lncRNA FOXP4-AS1 knockdown alleviated metastasis and EMT in NPC via miR-136-5p/MAPK1, indicating that lncRNA FOXP4-AS1 may be a valuable therapeutic target for NPC diagnosis and treatment.
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spelling pubmed-105696752023-10-13 LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1 Yan, Jin Zhou, Qi Anticancer Drugs Pre-Clinical Reports Nasopharyngeal carcinoma (NPC) is a malignant tumor caused by nasopharyngeal epithelium. Long non-coding RNAs (lncRNAs) and microRNAs have been identified as vital regulators in many tumors, including NPC. This study aimed to explain the biological roles and relevant mechanisms of lncRNA FOXP4-AS1 (FOXP4-AS1) in NPC. The levels of lncRNA FOXP4-AS1, miR-136-5p and MAPK1 in C666-1 and NP69 cells were analyzed by quantitative reverse transcription PCR (qRT-PCR). C666-1 cells viability, migration and invasion were evaluated by MTT and Transwell assay, respectively. The target gene of miR-136-5p predicted by TargetScan was further verified using dual luciferase reporter assay. Moreover, qRT-PCR and Western blot were adopted to assess epithelial–mesenchymal transition (EMT)-related gene expression, including E-cadherin and N-cadherin. We found that lncRNA FOXP4-AS1 was upregulated, while miR-136-5p was low-expressed in C666-1 cells, as opposed to NP69. Knockdown of FOXP4-AS1 notably suppressed C666-1 cell growth, inhibited cell migration and invasion. We also observed that E-cadherin expression was fortified and N-cadherin level was decreased in C666-1 cells after FOXP4-AS1-siRNA transfection. However, all these findings were eliminated in C666-1 cells after miR-136-5p inhibitor treatment. We also found miR-136-5p directly targeted MAPK1 and correlated inversely with MAPK1 expression in C666-1 cells. Further investigation suggested that MAPK1-plasmid reversed the effects of miR-136-5p mimic on cells viability, migration, invasion and EMT. To conclude, our data revealed that lncRNA FOXP4-AS1 knockdown alleviated metastasis and EMT in NPC via miR-136-5p/MAPK1, indicating that lncRNA FOXP4-AS1 may be a valuable therapeutic target for NPC diagnosis and treatment. Lippincott Williams & Wilkins 2023-11 2023-03-24 /pmc/articles/PMC10569675/ /pubmed/36961080 http://dx.doi.org/10.1097/CAD.0000000000001510 Text en Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND) (https://creativecommons.org/licenses/by-nc-nd/4.0/) , where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.
spellingShingle Pre-Clinical Reports
Yan, Jin
Zhou, Qi
LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1
title LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1
title_full LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1
title_fullStr LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1
title_full_unstemmed LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1
title_short LncRNA FOXP4-AS1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via miR-136-5p/MAPK1
title_sort lncrna foxp4-as1 silencing inhibits metastasis and epithelial–mesenchymal transition in nasopharyngeal carcinoma via mir-136-5p/mapk1
topic Pre-Clinical Reports
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10569675/
https://www.ncbi.nlm.nih.gov/pubmed/36961080
http://dx.doi.org/10.1097/CAD.0000000000001510
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