Azin1, or Antizyme Inhibitor 1, is a cell cycle regulator [1]. It can bind to and inhibit antizyme, a protein that normally functions as an anti-tumor regulator by deactivating growth-promoting proteins such as c-Myc [1].

In medulloblastoma, overexpression of AZIN1 in cells induces phenotypically aggressive features, while knocking-out AZIN1 in tumors via CRISPR-Cas9 in nude mice corresponds with reduced tumor progression and prolonged survival, and its expression directly correlates with MYC amplification status in patients [1]. In colorectal cancer, high levels of AZIN1 RNA editing are associated with poor prognosis, and edited AZIN1 enhances stemness and drives metastasis [2]. In endometrial cancer, ADAR1 expression is correlated with AZIN1 RNA editing level, and both are independent predictors of prognosis, with knockdown of ADAR1 leading to increased apoptosis in cancer cells [3]. In gastric cancer, ADAR1 knockout inhibits cell metastasis and reverses cisplatin resistance by down-regulating AZIN1 expression [4].

In conclusion, Azin1 plays a crucial role in tumor-related biological processes. Gene knockout models, especially in mice, have revealed its significant impact on the pathogenesis and progression of various cancers, including medulloblastoma, colorectal, endometrial, and gastric cancers, highlighting its potential as a biomarker and therapeutic target.