TTLL12, a member of the Tubulin Tyrosine Ligase-Like (TTLL) family, has functions in histone methylation and affects tubulin tyrosine ligase activities. It is involved in pathways related to cell polarization, ciliogenesis, antiviral response, and cancer progression. It uniquely affects tubulin post-translational modifications (PTMs) by promoting microtubule lysine acetylation and arginine methylation [2,4].

In ovarian cancer, TTLL12 expression is significantly increased in cancer tissues and cell lines compared to normal tissues and cell lines. Its expression level is associated with FIGO stage and peritoneal cytology, and is an independent risk factor for overall survival and disease-free survival of patients, suggesting it as a potential molecular marker for predicting ovarian cancer invasion and progression [1].

In polarized renal epithelial cells, TTLL12 localizes to the base of primary cilia and is required for cilia formation, as it binds to the α/β-tubulin heterodimer and regulates microtubule dynamics, stability, and PTMs [2,4]. Also, TTLL12 acts as a negative regulator of RNA-virus-induced type I IFN expression by inhibiting the interaction of VISA with other proteins in the antiviral signaling pathway [3].

In summary, TTLL12 plays essential roles in cilia formation, antiviral responses, and cancer-related processes. Studies in relevant models have provided insights into its functions in these biological and disease-related contexts, with its potential as a biomarker in ovarian cancer and its role in cilia and antiviral pathways being key findings.