ArticleFrontiers in oncology2026
GATA2-driven ZNF486-JAM2 activation collaboratively counteracts epithelial-mesenchymal transition and
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To investigate the role and molecular mechanism of the GATA2/ZNF486/JAM2 transcriptional regulatory axis in the invasion and migration of Uterine Corpus Endometrial Carcinoma (UCEC). Methods: We employed reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot (WB) to assess the expression levels of ZNF486, GATA2, and JAM2 in UCEC cell lines. Lentivirus-mediated overexpression and knockdown cell lines were established, and CCK-8, colony formation, Transwell, and wound healing assays were performed to evaluate cell proliferation, invasion, and migration. WB and immunofluorescence were used to detect changes in epithelial-mesenchymal transition (EMT) markers. The direct binding and transcriptional activation of target gene promoters by transcription factors were confirmed through ChIP-qPCR and dual-luciferase reporter assays. Results: ZNF486 was significantly downregulated in UCEC. Its overexpression upregulated E-cadherin, downregulated N-cadherin and Vimentin, and markedly inhibited cell proliferation, invasion, and migration. Mechanistically, ZNF486 directly bound to and transcriptionally activated the JAM2 promoter; knockdown of JAM2 partially attenuated the tumor-suppressive effects of ZNF486. Furthermore, GATA2 was identified as an upstream transcription factor that directly activated ZNF486 transcription; knockdown of ZNF486 abrogated the tumor-suppressive effects induced by GATA2 overexpression. Conclusion: GATA2 inhibits EMT, invasion, and migration in UCEC by transcriptionally activating the ZNF486-JAM2 axis. This pathway provides a potential molecular framework for understanding UCEC progression.
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