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AC010883.5 promotes cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition in cervical cancer by modulating the MAPK signaling pathway
Homo sapiens chromosome 2 clone RP11-339H12 (AC010883.5) is a dysregulated long non-coding RNA (lncRNA) that has never been investigated in cervical cancer (CC). Thus, the potential function and molecular mechanism remain unclear. Our study explored the biological function of AC010883.5 to determine...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10120252/ https://www.ncbi.nlm.nih.gov/pubmed/37081411 http://dx.doi.org/10.1186/s12885-023-10825-2 |
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author | Gan, Qiyu Huang, Xia Zhao, Wenrong Liu, Hui Xu, Yan Zhang, Xiaohua Cheng, Jingxin Chen, Rui |
author_facet | Gan, Qiyu Huang, Xia Zhao, Wenrong Liu, Hui Xu, Yan Zhang, Xiaohua Cheng, Jingxin Chen, Rui |
author_sort | Gan, Qiyu |
collection | PubMed |
description | Homo sapiens chromosome 2 clone RP11-339H12 (AC010883.5) is a dysregulated long non-coding RNA (lncRNA) that has never been investigated in cervical cancer (CC). Thus, the potential function and molecular mechanism remain unclear. Our study explored the biological function of AC010883.5 to determine the underlying mechanisms in CC and provide potential therapeutic targets for improving the clinical treatment strategy. We used quantitative real-time polymerase chain reaction to measure mitochondrial RNA levels and western blot to measure the protein levels of target genes. Further, we used Cell Counting Kit-8 and 5‐Bromo-2'-deoxyuridine incorporation assays to evaluate cell proliferation in vitro. Cell apoptosis was analyzed by flow cytometry. Cell invasion was analyzed by wound healing and Transwell migration assays was ued to analyze cell migration. Finally, the biological function and mechanism of AC010883.5 in CC growth were evaluated by in vivo xenograft assay. AC010883.5 was enhanced in CC tissues and cell lines, and enhanced AC010883.5 expression accelerated CC cell proliferation, migration, and invasion and induced epithelial–mesenchymal transition in vitro and in vivo. AC010883.5 also activated the mitogen-activated protein kinase (MAPK) signaling pathway by promoting phosphorylation of extracellular signal-regulated kinase 1/2 (i.e., ERK1/2) and MAPK kinase 1/2 (i.e., MEK1/2). Blocking the MAPK signaling pathway could counteract the pro-proliferative, pro-migrative, and pro-invasive effects of AC010883.5 over-expression. We found that the lncRNA, AC010883.5, is an oncogenic molecule involved in CC tumor progression via dysregulation of the MAPK signaling pathway, implying that AC010883.5 could be a tumor progression and therapeutic response biomarker. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-023-10825-2. |
format | Online Article Text |
id | pubmed-10120252 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-101202522023-04-22 AC010883.5 promotes cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition in cervical cancer by modulating the MAPK signaling pathway Gan, Qiyu Huang, Xia Zhao, Wenrong Liu, Hui Xu, Yan Zhang, Xiaohua Cheng, Jingxin Chen, Rui BMC Cancer Research Homo sapiens chromosome 2 clone RP11-339H12 (AC010883.5) is a dysregulated long non-coding RNA (lncRNA) that has never been investigated in cervical cancer (CC). Thus, the potential function and molecular mechanism remain unclear. Our study explored the biological function of AC010883.5 to determine the underlying mechanisms in CC and provide potential therapeutic targets for improving the clinical treatment strategy. We used quantitative real-time polymerase chain reaction to measure mitochondrial RNA levels and western blot to measure the protein levels of target genes. Further, we used Cell Counting Kit-8 and 5‐Bromo-2'-deoxyuridine incorporation assays to evaluate cell proliferation in vitro. Cell apoptosis was analyzed by flow cytometry. Cell invasion was analyzed by wound healing and Transwell migration assays was ued to analyze cell migration. Finally, the biological function and mechanism of AC010883.5 in CC growth were evaluated by in vivo xenograft assay. AC010883.5 was enhanced in CC tissues and cell lines, and enhanced AC010883.5 expression accelerated CC cell proliferation, migration, and invasion and induced epithelial–mesenchymal transition in vitro and in vivo. AC010883.5 also activated the mitogen-activated protein kinase (MAPK) signaling pathway by promoting phosphorylation of extracellular signal-regulated kinase 1/2 (i.e., ERK1/2) and MAPK kinase 1/2 (i.e., MEK1/2). Blocking the MAPK signaling pathway could counteract the pro-proliferative, pro-migrative, and pro-invasive effects of AC010883.5 over-expression. We found that the lncRNA, AC010883.5, is an oncogenic molecule involved in CC tumor progression via dysregulation of the MAPK signaling pathway, implying that AC010883.5 could be a tumor progression and therapeutic response biomarker. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-023-10825-2. BioMed Central 2023-04-21 /pmc/articles/PMC10120252/ /pubmed/37081411 http://dx.doi.org/10.1186/s12885-023-10825-2 Text en © The Author(s) 2023 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 Gan, Qiyu Huang, Xia Zhao, Wenrong Liu, Hui Xu, Yan Zhang, Xiaohua Cheng, Jingxin Chen, Rui AC010883.5 promotes cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition in cervical cancer by modulating the MAPK signaling pathway |
title | AC010883.5 promotes cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition in cervical cancer by modulating the MAPK signaling pathway |
title_full | AC010883.5 promotes cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition in cervical cancer by modulating the MAPK signaling pathway |
title_fullStr | AC010883.5 promotes cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition in cervical cancer by modulating the MAPK signaling pathway |
title_full_unstemmed | AC010883.5 promotes cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition in cervical cancer by modulating the MAPK signaling pathway |
title_short | AC010883.5 promotes cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition in cervical cancer by modulating the MAPK signaling pathway |
title_sort | ac010883.5 promotes cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition in cervical cancer by modulating the mapk signaling pathway |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10120252/ https://www.ncbi.nlm.nih.gov/pubmed/37081411 http://dx.doi.org/10.1186/s12885-023-10825-2 |
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