Mir21a, a microRNA, is involved in numerous biological processes and disease-related pathways. MicroRNAs regulate gene expression at the post-transcriptional level, and Mir21a has been implicated in pathways such as the NF-κB signaling pathway, which is crucial for inflammation and immune response [1,2,4]. It is also associated with cancer-related processes, making it of great biological importance. Genetic models, especially knockout (KO) mouse models, have been instrumental in understanding its function.

In colorectal cancer, Fusobacterium nucleatum activates Toll-like receptor 4 signaling to NF-κB, up-regulating Mir21a expression. Mir21a promotes cell proliferation and tumor development by reducing levels of the RAS GTPase RASA1. MiR21a-/-mice have fewer and smaller colorectal tumors, later appearance of fecal blood and diarrhea, and longer survival times compared to control mice, indicating its pro-tumorigenic role in this context [1]. In glioblastoma, targeting mmu-miR-21a with a single adeno-associated virus vector using CRISPR leads to lowered mmu-miR-21a levels in the brain, reduced tumor growth, and improved overall survival in glioblastoma-bearing mice, suggesting its importance in glioblastoma progression [3].

In conclusion, Mir21a plays essential roles in biological processes, especially in inflammation-related and cancer-associated pathways. Gene knockout mouse models, like the miR21a-/-mice in colorectal cancer and the targeting of mmu-miR-21a in glioblastoma, have significantly contributed to understanding its role in these disease areas, highlighting its potential as a therapeutic target in cancer treatment.