dGLYAT modulates Gadd45-mediated JNK activation and cell invasion

BACKGROUND: Cell invasion is a crucial step of tumor metastasis, finding new regulators of which offers potential drug targets for cancer therapy. Aberrant GLYAT expression is associated with human cancers, yet its role in cancer remains unknown. This study aims to understand the function and mechan...

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Autores principales: Xu, Meng, Ren, Pu, Tian, Juhui, Xiao, Lisha, Hu, Ping, Chen, Ping, Li, Wenzhe, Xue, Lei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9357319/
https://www.ncbi.nlm.nih.gov/pubmed/35933447
http://dx.doi.org/10.1186/s13008-022-00080-5
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author Xu, Meng
Ren, Pu
Tian, Juhui
Xiao, Lisha
Hu, Ping
Chen, Ping
Li, Wenzhe
Xue, Lei
author_facet Xu, Meng
Ren, Pu
Tian, Juhui
Xiao, Lisha
Hu, Ping
Chen, Ping
Li, Wenzhe
Xue, Lei
author_sort Xu, Meng
collection PubMed
description BACKGROUND: Cell invasion is a crucial step of tumor metastasis, finding new regulators of which offers potential drug targets for cancer therapy. Aberrant GLYAT expression is associated with human cancers, yet its role in cancer remains unknown. This study aims to understand the function and mechanism of Drosophila GLYAT in cell invasion. RESULTS: We found that dGLYAT regulates Gadd45-mediated JNK pathway activation and cell invasion. Firstly, loss of dGLYAT suppressed scrib depletion- or Egr overexpression-induced JNK pathway activation and invasive cell migration. Secondary, mRNA-seq analysis identified Gadd45 as a potential transcriptional target of dGLYAT, as depletion of dGLYAT decreased Gadd45 mRNA level. Finally, Gadd45 knockdown suppressed scrib depletion-induced JNK pathway activation and cell invasion. CONCLUSIONS: These evidences reveal the role of dGLYAT and Gadd45 in JNK-dependent cell invasion, and provide insight for the roles of their human homologs in cancers. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13008-022-00080-5.
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spelling pubmed-93573192022-08-08 dGLYAT modulates Gadd45-mediated JNK activation and cell invasion Xu, Meng Ren, Pu Tian, Juhui Xiao, Lisha Hu, Ping Chen, Ping Li, Wenzhe Xue, Lei Cell Div Research BACKGROUND: Cell invasion is a crucial step of tumor metastasis, finding new regulators of which offers potential drug targets for cancer therapy. Aberrant GLYAT expression is associated with human cancers, yet its role in cancer remains unknown. This study aims to understand the function and mechanism of Drosophila GLYAT in cell invasion. RESULTS: We found that dGLYAT regulates Gadd45-mediated JNK pathway activation and cell invasion. Firstly, loss of dGLYAT suppressed scrib depletion- or Egr overexpression-induced JNK pathway activation and invasive cell migration. Secondary, mRNA-seq analysis identified Gadd45 as a potential transcriptional target of dGLYAT, as depletion of dGLYAT decreased Gadd45 mRNA level. Finally, Gadd45 knockdown suppressed scrib depletion-induced JNK pathway activation and cell invasion. CONCLUSIONS: These evidences reveal the role of dGLYAT and Gadd45 in JNK-dependent cell invasion, and provide insight for the roles of their human homologs in cancers. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13008-022-00080-5. BioMed Central 2022-08-06 /pmc/articles/PMC9357319/ /pubmed/35933447 http://dx.doi.org/10.1186/s13008-022-00080-5 Text en © The Author(s) 2022 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
Xu, Meng
Ren, Pu
Tian, Juhui
Xiao, Lisha
Hu, Ping
Chen, Ping
Li, Wenzhe
Xue, Lei
dGLYAT modulates Gadd45-mediated JNK activation and cell invasion
title dGLYAT modulates Gadd45-mediated JNK activation and cell invasion
title_full dGLYAT modulates Gadd45-mediated JNK activation and cell invasion
title_fullStr dGLYAT modulates Gadd45-mediated JNK activation and cell invasion
title_full_unstemmed dGLYAT modulates Gadd45-mediated JNK activation and cell invasion
title_short dGLYAT modulates Gadd45-mediated JNK activation and cell invasion
title_sort dglyat modulates gadd45-mediated jnk activation and cell invasion
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9357319/
https://www.ncbi.nlm.nih.gov/pubmed/35933447
http://dx.doi.org/10.1186/s13008-022-00080-5
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