SUMO2, a small ubiquitin-like modifier, plays a crucial role in modulating the stability and activity of other proteins. It is involved in multiple biological processes such as protein quality control, where it converges with ubiquitylation to mediate protein degradation, primarily through SUMO-targeted ubiquitin ligases [3]. SUMO2 is also engaged in post-translational modification pathways like SUMOylation, which is associated with DNA damage repair, immune responses, carcinogenesis, cell cycle progression, and apoptosis [5].

In murine preimplantation embryos, knockdown of SUMO2 using siRNA microinjection significantly reduced the rate of in vitro blastocyst development and altered the expression of key pluripotency genes like CDX2, OCT4, and NANOG, along with global H3K27me3 levels, indicating its importance in early embryo development [2].

In nasopharyngeal carcinoma, circRNF13 activated SUMO2 by binding to its 3'-UTR, and up-regulation of SUMO2 promoted GLUT1 degradation through SUMOylation and ubiquitination, regulating the AMPK-mTOR pathway by inhibiting glycolysis, ultimately affecting the proliferation and metastasis of the cancer [1].

In vascular endothelial function, SUMO2 expression was upregulated in hypercholesterolemic mice, impairing endothelium-dependent vasorelaxation, while inhibition of SUMO2 also impaired normal vasorelaxation in normocholesterolemic mice, suggesting its dual role in maintaining vascular homeostasis [4].

In conclusion, SUMO2 is essential for various biological functions, including embryo development, regulation of cancer-related processes, and maintenance of vascular endothelial function. Studies using gene knockdown models in mice have been instrumental in revealing these functions, providing insights into disease mechanisms such as embryo development disorders, cancer progression, and vascular diseases.