Snord3a, a small nucleolar RNA, is involved in multiple biological processes and diseases. It plays a role in regulating gene transcription and may be associated with pathways related to oxidative stress, inflammation, and cell death. Its study in genetic models can provide insights into its functions.

In acute kidney injury (AKI) mouse models, Snord3a deficiency alleviates renal injury. Snord3a regulates the STING signaling axis by promoting STING gene transcription, and its deficiency mitigates STING-associated ferroptosis phenotypes and tubular injury. Administration of Snord3a antisense oligonucleotides shows therapeutic advantage in AKI mouse models [1].

In breast cancer cells, overexpression of Snord3a specifically sensitizes cells to 5-fluorouracil (5-FU) by sponging miR-185-5p to enhance UMPS expression [2].

In leukemia, the transcription of Snord3a is increased upon leukemia transformation and enriched in leukemia stem cells. Suppression of Snord3a impairs leukemia cell proliferation and colony-forming capacity in AML cell lines and primary patient samples [3].

In conclusion, Snord3a is implicated in various disease conditions. The study of Snord3a in gene knockout (KO) or conditional knockout (CKO) mouse models has revealed its role in promoting ferroptosis in AKI, chemosensitization in breast cancer, and maintenance of leukemia propagation. These findings highlight its potential as a prognostic and therapeutic target in these diseases.