ArticleCell biology and toxicology2024
The pivotal role of ZNF384: driving the malignant behavior of serous ovarian cancer cells via the LIN28B/UBD axis.
Article in Cell biology and toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Ubiquitin D Correlates with Disease Severity and T Cell Infiltration in Cholestasis: Evidence from Integrated Bioinformatics and Experimental Analyses.International journal of medical sciences · 2026Article
- Transcriptomic analysis reveals the potential role of TOE1 in hepatocellular carcinoma.Scientific reports · 2025Article
- Pan-cancer multi-omics profiling reveals ubiquitin D as a novel biomarker for diagnosis, immune microenvironment remodeling and prognostic prediction.Discover oncology · 2025Article
- Cancer-associated fibroblasts-secreted lactate promotes RNA polymerase III subunit G-mediated epithelial-mesenchymal transition in non-small cell lung cancer by increasing m6A modification of zinc finger protein 384.Journal of cell communication and signaling · 2025Article
- Integrated Network Analysis Decipher ZNF384-Related miR-20b-5p and miR-424-5p in Colon Adenocarcinoma.Cancer reports (Hoboken, N.J.) · 2025Article
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6 authors.
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Abstract
Zinc finger protein 384 (ZNF384) is a highly conserved transcribed gene associated with the development of multiple tumors, however, its role and mechanism in serous ovarian cancer (SOC) are unknown. We first confirmed that ZNF384 was abnormally highly expressed in SOC tissues by bioinformatics analysis and immunohistochemistry. We further used lentivirus packaging and transfection techniques to construct ZNF384 overexpression or knockdown cell lines, and through a series of cell function experiments, gradually verified that ZNF384 promoted a series of malignant behaviors of SOC cell proliferation, migration, and invasion. By establishing a xenotransplantation model in nude mice, it was confirmed that ZNF384 promoted the progress of SOC in vivo. Mechanistically, Overexpression of ZNF384 enhanced the transcriptional activity of Lin-28 homolog B (LIN28B), which promoted the malignant behavior of SOC cells. In addition, LIN28B could regulate the expression of the downstream factor ubiquitin D (UBD) in SOC cells, further promoting the development of SOC. This study shows that ZNF384 aggravates the malignant behavior of SOC cells through the LIN28B/UBD axis, which may be used as a diagnostic biomarker for patients with SOC.
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