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Zinc finger protein 671 (ZNF671) is a nuclear transcription factor belonging to the KRAB (Krüppel-associated box) zinc finger protein family, characterized by C2H2-type zinc fingers and a KRAB domain[1][2]. It enables sequence-specific DNA binding and regulates gene expression by interacting with RNA polymerase II regulatory regions[1]. ZNF671 acts as a tumor suppressor in various cancers, such as bladder urothelial carcinoma, serous ovarian cancer, colorectal carcinoma, laryngeal squamous cell carcinoma, breast, lung, pancreas, and brain tumors; its function is often compromised by promoter hypermethylation leading to epigenetic silencing[1][2]. Loss of ZNF671 expression is associated with increased tumor proliferation, invasion, stemness, metastasis, and poor prognosis, while its restoration can suppress tumor growth partly by inhibiting signaling pathways such as Notch or MAPK6 and blocking epithelial-mesenchymal transition (EMT)[1][2]. ZNF671 methylation is emerging as a non-invasive biomarker for cancer detection and recurrence prediction[1]. There are currently no drugs known to target ZNF671 directly, and no clinically established mechanisms of action or safety concerns related to therapeutic modulation of this protein[1][2].
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