Tmub1, also known as HOPS, is a transmembrane and ubiquitin-like domain-containing protein. It is involved in multiple biological functions such as cell proliferation regulation, post-translational modification of proteins, and the endoplasmic reticulum-associated degradation pathway. It plays a role in important pathways like STAT3 signaling, immune-related pathways, and is associated with various biological processes and diseases [2,4,5].

In liver regeneration, Tmub1 overexpression vectors impaired mouse liver regeneration after partial hepatectomy. Loss-and gain-of-function analyses in human hepatocyte Lo2 cells showed that Tmub1 inhibits STAT3 phosphorylation and its signaling, suggesting a negative regulatory role in hepatocyte proliferation through STAT3 signaling [4].

In tumor-related studies, in vivo studies with mice found that a synthetic peptide engineered to compete with TMUB1 significantly promoted antitumor immunity and suppressed tumor growth. High TMUB1 protein levels in human tumor tissue correlate with PD-L1 expression, and are associated with poor patient survival rates, as TMUB1 modulates PD-L1 polyubiquitination and glycosylation to promote tumor immune evasion [1]. In colorectal cancer, high TMUB1 expression is related to a poor prognosis, and is associated with hypoxia, angiogenesis, and immune cell infiltration [3].

In conclusion, Tmub1 is a key regulator in multiple biological processes. Model-based research, especially in mouse models, has revealed its significance in liver regeneration and tumor-related diseases. Understanding Tmub1's functions provides potential strategies for the management of liver regeneration and treatment of certain tumors.