Authors
Yanke Zhang, Hongbin Zhu, Xueqin Wang, Wei Dong, Maoyu Zhang, Xinyue Song, Danye Han, Qian Chai, Xueyi Feng, Xiaozheng Wei, Hongyu Chen, Yonghuai Li, Lei Zhao, Qian Dai
Published in
Science China. Life sciences. Jun 24, 2026. Epub Jun 24, 2026.
Abstract
Non-small cell lung cancer (NSCLC) remains a significant global health challenge, making the exploration of potential therapeutic targets critically important. In this study, we discovered that ZNF200 is highly expressed in NSCLC tissues and plays an oncogenic role by promoting cell proliferation and metastasis both in vitro and in vivo. Mechanistically, ZNF200 recruits DDX17 to the promoter region of RBPJ to upregulate the expression of RBPJ and activate the Notch signaling pathway. ZNF200 and DDX17 increase H3K4me3 enrichment at the RBPJ promoter. Furthermore, ZNF200 interacts with SETD1A to regulate H3K4me3 deposition, sustaining the transcriptional activity of the RBPJ promoter. Interestingly, DDX17 could maintain the protein stability of ZNF200 by inhibiting the ubiquitin-proteasome degradation pathway, which further increased the expression level of ZNF200 in the nucleus. Additionally, we revealed that miR-139 inhibits ZNF200 expression and that the introduction of miR-139 abrogates the increased cell proliferation and metastasis caused by ZNF200 over-expression. Overall, our work demonstrates the critical role and molecular mechanism of ZNF200 in regulating NSCLC development, highlighting the potential of targeting ZNF200 as an effective strategy in NSCLC treatment.
PMID:
42364057
Bibliographic data and abstract were imported from PubMed on 27 Jun 2026.
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