{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMyeloid zinc finger 1 (MZF1) is a versatile transcription factor that, in many cancers, functions as an oncogenic activator. For example, in lung squamous cell carcinoma, FTO‐mediated demethylation lowers m6A levels and elevates MZF1 expression to promote tumor progression, while in colorectal and cervical cancer MZF1 directly activates the Axl receptor to enhance cell migration and invasion. In ErbB2‐positive breast cancer, MZF1 drives the transcription of cysteine cathepsin B via an enhancer element to facilitate invasiveness, and in lung adenocarcinoma, loss of LKB1 leads to a MZF1/MYC axis that fuels malignant growth. In addition, a recent review summarizes the broad oncogenic roles of MZF1 in solid tumors, including its regulation of ferroportin in prostate cancer, activation of matrix metalloproteinase‐14 in gastric cancer, stimulation of p55PIK transcription in colorectal cancer, promotion of fibroblast growth factor‐2 expression, and upregulation of the melanoma‐associated antigen PRAME."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn other contexts, MZF1 acts as a repressor or tumor‐suppressive modulator. In osteoblasts, for instance, MZF1 cooperates with Sp1/Sp3 to control N‑cadherin transcription. In cervical cancer, TGF‑β1–ERK1/2 signaling recruits MZF1 to the CK17 promoter, facilitating metastasis, yet MZF1 can also directly bind to and repress the MMP‑2 promoter to limit cell invasion. Its interaction with Elk‑1 has been implicated in the transcriptional upregulation of PKCα in hepatocellular carcinoma, whereas in endometrial cancer MZF1 binding to the hypermethylated PAX2 promoter contributes to its transcriptional repression. Moreover, by interacting with LDOC1, MZF1 enhances apoptosis, and its modulation of the MT2A–NF‑κB axis, activation of SMAD4 transcription, recruitment of CHD7 to the p16INK4A promoter, and the observation that loss of nuclear MZF1 correlates with aggressive oral squamous cell carcinoma, further underscore its context‐dependent inhibitory functions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMZF1 also plays pivotal roles in non‐oncogenic contexts by modulating differentiation and metabolic pathways. In stromal cells, calcitriol‑induced upregulation of MZF1 enhances GAPDH transcription, while in the hematopoietic niche it regulates connective tissue growth factor (CTGF) and NOV expression. Its function in triple‑negative breast cancer has been linked to enhanced cell migration and invasion, and in bladder transitional cell carcinoma MZF1 has been investigated for its association with PKCα expression. Furthermore, MZF1 regulates angiogenic and metabolic gene promoters—including those of VEGF and PYROXD2—and is essential for the transcriptional activation of glycosyltransferases such as hST6GalNAc IV in immune cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, genetic variations that influence MZF1 binding dynamics have been associated with altered inflammatory responses and Alzheimer’s disease risk, while recent evidence indicates that the MZF1/RBM3 axis affords neuroprotection against toxic insults in neuronal injury models. These findings highlight the diverse regulatory spectrum of MZF1, spanning from oncogenic stimulation and tumor suppression to roles in cellular differentiation, metabolism, and neuroprotection."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jiqin Liu, Dangli Ren, Zhenhua Du, et al. 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