Mmp2, a Zn2+-dependent metalloproteinase, is involved in various biological processes and diseases. It plays a role in extracellular matrix remodeling and is associated with pathways related to cancer and angiogenesis. Genetic models are valuable for studying its functions.

In melanoma, Mmp2 signals proinflammatory pathways on antigen-presenting cells via TLR2 and TLR4, promoting tumor growth. Overexpression of Mmp2 in B16 cells led to rapid tumor growth, reduced intratumoral cytolytic cells, and increased M2 macrophages, while knockdown of Mmp2 slowed tumor growth and enhanced T-cell proliferation and NK-cell recruitment [1]. In breast cancer, Mmp2 overexpression was associated with an unfavorable overall survival and a higher risk of distant metastasis [2]. In prostate cancer, the MMP2-1306C/T polymorphism might increase the cancer risk, especially in the Asian population [3]. In gastric cancer, abnormal Mmp2 expression was associated with a shorter overall survival in both Caucasian and Asian populations [4]. In dilated cardiomyopathy, MMP2 gene polymorphisms were associated with disease susceptibility and prognosis in the Chinese Han population [5]. In polycystic ovary syndrome, two MMP2 gene polymorphisms (rs7201 and rs243849) were found to be associated with a reduced risk of the disease [6].

In conclusion, Mmp2 is a key metalloproteinase involved in multiple disease conditions such as cancer, cardiovascular, and reproductive diseases. Mouse models, including potential KO/CKO models, have been crucial in revealing its role in tumorigenesis, metastasis, and disease susceptibility, providing insights into the underlying molecular mechanisms and potential therapeutic targets.