Meox2, or Mesenchyme Homeobox 2, is a transcription factor involved in mesoderm differentiation, with functions in the development of bones, muscles, vasculature, and dermatomes [4]. It has been associated with multiple signaling pathways, such as ERK/MAPK, PI3K/AKT, and is important in various biological processes and disease contexts. Genetic models, like mouse models, have been crucial in studying its functions.

In gliomas, Meox2 has been shown to act as an oncogenic transcription regulator. Knockdown of Meox2 in patient-derived GBM tumorspheres inhibited cell proliferation and affected ERK phosphorylation [1]. In glioma cells, its inhibition changed cell morphology, inhibited cell proliferation, motility, EMT, focal adhesion formation, and F-actin assembly, suggesting its role in tumorigenesis and progression [2]. In DBA/2J glaucoma mouse models, Meox2 haploinsufficiency accelerated axonal degeneration, indicating its role in controlling IOP-dependent vascular remodeling and neuroinflammation to promote axon survival [3]. In glioma stem-like cells, loss of function of Meox2 via siRNA affected cell viability, proliferation, and correlated with cell differentiation and changes in adhesion-related proteins [5].

In conclusion, Meox2 is a significant transcription factor involved in mesoderm-related development and plays important roles in diseases such as gliomas and glaucoma. Mouse models, especially those with gene knockout or haploinsufficiency, have been instrumental in revealing its functions in these disease conditions, helping to understand the underlying biological mechanisms and potentially providing new therapeutic targets.