Snord3a is a small nucleolar RNA that has been implicated in multiple biological processes and disease conditions. It plays roles in pathways related to oxidative stress, inflammation, and may be involved in ribosome biogenesis as small nucleolar RNAs are generally associated with such functions [3,4].

In acute kidney injury (AKI) mouse models, Snord3a deficiency alleviates renal injury. Snord3a regulates the stimulator of interferon genes (STING) signaling axis by promoting STING gene transcription, and its deficiency mitigates STING-associated ferroptosis phenotypes and tubular injury progression. Administration of Snord3a antisense oligonucleotides shows therapeutic advantage in AKI mouse models, highlighting its potential as a prognostic and therapeutic target for AKI [1].

In breast cancer, overexpression of Snord3a specifically sensitizes breast cancer cells to 5-fluorouracil (5-FU) by sponging miR-185-5p to enhance uridine monophosphate synthetase (UMPS) protein expression, suggesting it could be a biomarker and therapeutic target to improve 5-FU-based chemotherapy efficacy [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, with less impact on healthy CD34+ hematopoietic stem and progenitor cells [3].

In conclusion, Snord3a is involved in diverse biological functions across different disease areas. Gene knockout or knockdown models in mice and cell lines have been crucial in revealing its role in AKI, breast cancer, and leukemia, indicating its potential as a biomarker and therapeutic target in these diseases.