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 mechani...

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Bibliographic Details
Published in:Cell division 2022-08, Vol.17 (1), p.1-4, Article 4
Main Authors: Xu, Meng, Ren, Pu, Tian, Juhui, Xiao, Lisha, Hu, Ping, Chen, Ping, Li, Wenzhe, Xue, Lei
Format: Article
Language:English
Subjects:
Apoptosis
Cell activation
Cell adhesion & migration
Cell cycle
Cell invasion
Cell migration
dGLYAT
Drosophila
Fatalities
Gadd45
GADD45 protein
Genes
Insects
Invasiveness
JNK
Kinases
Liver cancer
Metastases
Metastasis
Proteins
Therapeutic targets
Tumors
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Summary: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.
ISSN:1747-1028
1747-1028
DOI:10.1186/s13008-022-00080-5