Dzip3, also known as DAZ-interacting zinc finger 3, is an RNA-binding RING-type ubiquitin ligase. It is involved in multiple physiological functions, such as regulating chemokine-or estradiol-induced gene expression, self-renewal, and maintaining pluripotency in mouse embryonic stem cells. It also participates in epigenetic regulation, like histone H2A ubiquitination, and is associated with pathways related to cell-cycle regulation and cancer progression [4,5,6].

In glioma, lower DZIP3 expression is related to malignancy, and it serves as an independent predictive factor of good prognosis. Gene enrichment analysis indicated it affects glioma biological behavior through the angiogenesis pathway. In IDH1 wild-type lower-grade gliomas, DZIP3 expression can stratify patients into two groups with different survival times [1].

In gastric cancer, DZIP3 is significantly up-regulated, promoting cell proliferation and metastasis. Its higher expression is associated with poor prognosis. Proteomic and transcriptome analyses showed its interaction with epigenetic regulators and its impact on genes crucial for tumors [2].

In cancer cell models, DZIP3 promoted tumor growth and metastasis. Depletion of DZIP3 led to reduced Cyclin D1 expression, G1 arrest, and defective cell growth. DZIP3 stabilizes Cyclin D1 at both mRNA and protein levels in a cell-cycle phase-dependent manner [3].

In addition, the 1st exon DNA methylation of DZIP3 can predict the onset of early-stage and all pTNM stages of colorectal cancer [7].

In conclusion, Dzip3 is a key factor in multiple biological processes and disease conditions. Its functions in promoting cell-cycle progression, as well as its role in cancer development and progression, are well-demonstrated through various in vivo and in vitro studies. The research on Dzip3 provides valuable insights into the mechanisms of cancer and other diseases, offering potential targets for treatment.