Syt12, or Synaptotagmin 12, is a member of the synaptotagmins family. It is an abundant synaptic vesicle protein not binding Ca(2+), and is phosphorylated by cAMP-dependent protein kinase-A at serine-97 in an activity-dependent manner, suggesting its involvement in cAMP-dependent synaptic plasticity [5].

In cancer research, Syt12 has been found to play oncogenic roles. In thyroid carcinoma, it is significantly overexpressed, promoting carcinoma progression and metastasis, and is a potential biomarker for diagnosis and treatment in papillary thyroid cancer (PTC) [1]. In oral squamous cell carcinoma (OSCC), Syt12 is up-regulated, and its knockdown leads to depressed cellular proliferation, migration, and invasion with cell cycle arrest at G1 phase, suggesting its significance in OSCC progression [2]. In gastric cancer, it may promote the proliferation and migration of gastric cancer cells by inducing epithelial-mesenchymal transition (EMT), and is associated with clinicopathological features, immune cell infiltration, and prognosis [3]. In lung adenocarcinoma, its expression is increased, associated with advanced tumor stage and reduced prognosis, and it promotes cell proliferation and migration via the PI3K/AKT/mTOR pathway [4].

In conclusion, Syt12 is essential for cAMP-dependent presynaptic long-term potentiation (LTP) at mossy-fiber synapses in the hippocampus. In cancer, Syt12 acts as an oncogene promoting the progression of multiple cancers including thyroid, oral, gastric, and lung adenocarcinoma, highlighting its potential as a biomarker and therapeutic target in these diseases.