ArticleFrontiers in cellular and infection microbiology2024
KIF20A activated by transcription factor GATA2 promotes cell growth in hepatitis B virus-related hepatocellular carcinoma.
Article in Frontiers in cellular and infection microbiology, 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.
- GATA2 promotes hepatitis B virus-associated hepatocellular carcinoma development by regulating AURKA.Archives of microbiology · 2026Article
- Transcription factor HOXA4 promotes HBV replication and hepatocellular carcinoma proliferation by activating KIF11 transcription.In vitro cellular & developmental biology. Animal · 2026Article
- KIF20A promotes cervical cancer progression by interacting with CLIP1.Scientific reports · 2026Article
- Article
- Nitidine chloride may mediate its antitumor effects by targeting kinesin family member 20A in colorectal cancer cells.World journal of clinical oncology · 2025Article
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Authors and funding
13 authors.
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Abstract
Background: Elevated evidence suggests that KIF20A plays an important role in hepatocellular carcinoma (HCC) progression. Nevertheless, the underlying mechanism by which KIF20A promotes HCC cell growth are not well understood. Methods: Using TCGA-LIHC RNAseq and GEO datasets, we assessed the KIF20A expression and patient survival in HCC and hepatitis B virus (HBV)-related HCC. Mutant and CNV analysis were performed to evaluate the genetic alteration of KIF20A in HCC. PPI network and GSEA enrichment was utilized for analyzing the KIF20A-related genes and involved pathways in HCC. To further explore regulatory mechanism in HBV-related HCC, PROMO prediction and luciferase reporter system was utilized for verifying HBx/GATA2/KIF20A binding sites. CCK-8 and flow cytometry were carried out to determine the regulation of GATA2-KIF20A on HBV-related HCC cell proliferation and apoptosis. Results: KIF20A was significantly upregulated in pan-cancer (including HCC). KIF20A mRNA level was a significant independent predictor of overall survival in HBV-related HCC patients. Genetic alterations analysis revealed the copy number gain and amplification triggered KIF20A upregulation in HCC. In addition, the genes associated with KIF20A expression in HCC was enriched in PLK1 pathway and cell cycle in HCC. HBx might indirectly binds to KIF20A promoter via regulating GATA2. Additionally, transcription factor GATA2 directly binds to the promoter region of KIF20A. Overexpression of GATA2 promotes HepG2.2.15 cell growth and inhibits cell apoptosis via modulating KIF20A. Conclusions: Our findings demonstrated that HBx contributed to cell proliferation by interacting with GATA2 and KIF20A in HBV-related HCC.
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