Mir155, also known as microRNA-155, is a key regulator involved in various biological processes. It has been implicated in immune cell development and function, and is associated with pathways related to inflammation, tumorigenesis, and tissue homeostasis. Genetic models, such as KO mouse models, have been crucial in elucidating its functions.

In the MMTV-PyMT mouse model, miR155 deficiency led to reduced breast tumor burden, with decreased tumor volume, number, and weight. This was accompanied by increased apoptosis, decreased proliferation, and modulation of the tumor microenvironment, including reduced expression of macrophage markers associated with protumorigenic processes [1].

In Mir155-Tg and Mir155-KO mice, miR155 was found to regulate osteogenesis and bone mass phenotype. Mir155-Tg mice had a low bone mass phenotype, while Mir155-KO mice showed a high bone mass phenotype and better bone regeneration. miR155 exerted its effect via targeting S1pr1 gene [2].

In vascular smooth muscle cells, miR155 deficiency attenuated vascular calcification by increasing Akt phosphorylation and FOXO3a degradation, and thus reducing VSMC apoptosis induced by calcification medium [3].

In conclusion, Mir155 plays diverse and significant roles in biological processes and disease conditions. The use of Mir155 KO mouse models has provided valuable insights into its functions in breast cancer, osteogenesis, and vascular calcification, among others. These findings contribute to a better understanding of the underlying mechanisms and may offer potential targets for therapeutic intervention.