TMEM88, a double-transmembrane protein, is involved in regulating cell proliferation, differentiation, apoptosis and tumor progression. It mediates different signaling pathways, most notably the Wnt/β-catenin signaling pathway, and its dysregulation has been associated with various biological processes and diseases [1,2,3,4,5,6,7,8,9,10].

In bladder cancer, upregulation of TMEM88 decreased cellular proliferative and invasive abilities by downregulating the Wnt/β-catenin pathway, as it decreased the level of active β-catenin and prohibited pathway activation through downregulating GSK-3β phosphorylation [2]. In non-alcoholic fatty liver disease (NAFLD), TMEM88 modulated lipid synthesis and metabolism cytokine secretion by regulating the Wnt/β-catenin signaling pathway. Transfection with pEGFP-C1-TMEM88 upregulated PPAR-α and ACOX-1, and downregulated SREBP-1c and FASN [6]. In keloid fibroblasts, TMEM88 overexpression inhibited cell proliferation, migration and extracellular matrix expression through inactivating the Wnt/β-catenin signaling pathway [9].

In conclusion, TMEM88 plays a crucial role in multiple biological processes mainly through its regulation of the Wnt/β-catenin signaling pathway. Its functions are evident in diseases such as bladder cancer, NAFLD and keloid formation, highlighting its potential as a therapeutic target. Research on TMEM88, especially through gene-related models, helps in understanding disease mechanisms and developing new treatment strategies.