ArticleScientific reports2023
ZNF143 facilitates the growth and migration of glioma cells by regulating KPNA2-mediated Hippo signalling.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- ZNF143 suppresses mitophagy to drive MASLD progression by regulating SMURF1/TRPV1 axis.Molecular genetics and genomics : MGG · 2026Article
- Positive TAZ-TDG feedback loop drives proneural-to-mesenchymal transition to promote glioblastoma progression.Journal of translational medicine · 2026Article
- A plant alkaloid lycorine inhibits non-small cell lung cancer cell proliferation, metastasis, glycolysis and promotes ferroptosis through the ZNF143/SPC25 axis.Journal of natural medicines · 2026Article
- RBM24 Suppresses the Tumorigenesis of Glioblastoma by Stabilizing LATS1 mRNA.Biochemical genetics · 2025Article
- HDAC4/MybL1/YAP novel signaling axis is required for pancreatic cancer metastasis to the liver.International journal of biological sciences · 2025Article
- Exploring the significance and potential mechanisms of hippo pathway-associated genes in prognosis of glioma patients.Discover oncology · 2024Article
- Identification of Key Immune and Cell Cycle Modules and Prognostic Genes for Glioma Patients through Transcriptome Analysis.Pharmaceuticals (Basel, Switzerland) · 2024Article
- SFINN: inferring gene regulatory network from single-cell and spatial transcriptomic data with shared factor neighborhood and integrated neural network.Bioinformatics (Oxford, England) · 2024Article
- Epigenetic silencing ofEpigenomics · 2024Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The disordered expression of ZNF143 is closely related to the malignant progression of tumours. However, the basic control mechanism of ZNF143 in glioma has not yet been clarified. Therefore, we tried to find a new pathway to illustrate the function of ZNF143 in glioma. To explore the function of KPNA2 in the development of glioma, we used survival analysis by the Kaplan‒Meier method to assess the overall survival (OS) of patients with low and high KPNA2 expression in the TCGA and CGGA cohorts. Western blotting assays and RT‒PCR assays were utilized to determine the expression level of KPNA2 in glioma cells. The interaction between ZNF143 and KPNA2 was confirmed by ChIP assays. Proliferation was assessed by CCK-8 assays, and migration was evaluated by wound healing and Transwell assays. Apoptosis was determined by flow cytometry, and the expression level of YAP/TAZ was visualized using an immunofluorescence assay. The expression levels of LATS1, LATS2, YAP1, and p-YAP1 were determined. Patients with low KPNA2 expression showed a better prognosis than those with high KPNA2 expression. KPNA2 was found to be upregulated in human glioma cells. ZNF143 can bind to the promoter region of KPNA2. Downregulation of ZNF143 and KPNA2 can activate the Hippo signalling pathway and reduce YAP/TAZ expression in human glioma cells, thus inducing apoptosis of human glioma cells and weakening their proliferation, migration and invasion. In conclusion, ZNF143 mediates the Hippo/YAP signalling pathway and inhibits the growth and migration of glioma cells by regulating KPNA2.
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