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UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway
Ubiquitin-associated protein 2-like (UBAP2L) is highly expressed in various types of tumors and has been shown to participate in tumor growth and metastasis; however, its role in gastric cancer (GC) remains unknown. In this study, we observed that UBAP2L expression was markedly elevated in GC tissue...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8933503/ https://www.ncbi.nlm.nih.gov/pubmed/35304439 http://dx.doi.org/10.1038/s41420-022-00916-7 |
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author | Li, Ou Zhao, Cheng Zhang, Jian Li, Feng-Nan Yang, Zi-Yi Liu, Shi-Lei Cai, Chen Jia, Zi-Yao Gong, Wei Shu, Yi-Jun Dong, Ping |
author_facet | Li, Ou Zhao, Cheng Zhang, Jian Li, Feng-Nan Yang, Zi-Yi Liu, Shi-Lei Cai, Chen Jia, Zi-Yao Gong, Wei Shu, Yi-Jun Dong, Ping |
author_sort | Li, Ou |
collection | PubMed |
description | Ubiquitin-associated protein 2-like (UBAP2L) is highly expressed in various types of tumors and has been shown to participate in tumor growth and metastasis; however, its role in gastric cancer (GC) remains unknown. In this study, we observed that UBAP2L expression was markedly elevated in GC tissues and five GC cell lines. Higher expression of UBAP2L was associated with poor prognosis as revealed by bioinformatics analysis on online websites and laboratory experiments. Knockdown of UBAP2L impeded the migration and invasion abilities of GC cell lines. In contrast, its overexpression enhanced the migration and invasion abilities of GC cell lines. Overexpression of UBAP2L also increased the number and size of lung metastatic nodules in vivo. According to the results of mass spectrometry and pathway annotation of the identified proteins, the PI3K/AKT pathway was found to be related to UBAP2L regulation. Further exploration and rescue experiments revealed that UBAP2L stimulates the expression and nuclear aggregation of p65 and promotes the expression of SP1 by activating the PI3K/AKT pathway. In summary, our findings indicate that UBAP2L regulates GC metastasis through the PI3K/AKT/SP1/NF-κB axis. Thus, targeting UBAP2L may be a potential therapeutic strategy for GC. |
format | Online Article Text |
id | pubmed-8933503 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-89335032022-04-01 UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway Li, Ou Zhao, Cheng Zhang, Jian Li, Feng-Nan Yang, Zi-Yi Liu, Shi-Lei Cai, Chen Jia, Zi-Yao Gong, Wei Shu, Yi-Jun Dong, Ping Cell Death Discov Article Ubiquitin-associated protein 2-like (UBAP2L) is highly expressed in various types of tumors and has been shown to participate in tumor growth and metastasis; however, its role in gastric cancer (GC) remains unknown. In this study, we observed that UBAP2L expression was markedly elevated in GC tissues and five GC cell lines. Higher expression of UBAP2L was associated with poor prognosis as revealed by bioinformatics analysis on online websites and laboratory experiments. Knockdown of UBAP2L impeded the migration and invasion abilities of GC cell lines. In contrast, its overexpression enhanced the migration and invasion abilities of GC cell lines. Overexpression of UBAP2L also increased the number and size of lung metastatic nodules in vivo. According to the results of mass spectrometry and pathway annotation of the identified proteins, the PI3K/AKT pathway was found to be related to UBAP2L regulation. Further exploration and rescue experiments revealed that UBAP2L stimulates the expression and nuclear aggregation of p65 and promotes the expression of SP1 by activating the PI3K/AKT pathway. In summary, our findings indicate that UBAP2L regulates GC metastasis through the PI3K/AKT/SP1/NF-κB axis. Thus, targeting UBAP2L may be a potential therapeutic strategy for GC. Nature Publishing Group UK 2022-03-19 /pmc/articles/PMC8933503/ /pubmed/35304439 http://dx.doi.org/10.1038/s41420-022-00916-7 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Li, Ou Zhao, Cheng Zhang, Jian Li, Feng-Nan Yang, Zi-Yi Liu, Shi-Lei Cai, Chen Jia, Zi-Yao Gong, Wei Shu, Yi-Jun Dong, Ping UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway |
title | UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway |
title_full | UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway |
title_fullStr | UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway |
title_full_unstemmed | UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway |
title_short | UBAP2L promotes gastric cancer metastasis by activating NF-κB through PI3K/AKT pathway |
title_sort | ubap2l promotes gastric cancer metastasis by activating nf-κb through pi3k/akt pathway |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8933503/ https://www.ncbi.nlm.nih.gov/pubmed/35304439 http://dx.doi.org/10.1038/s41420-022-00916-7 |
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