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. It plays a role in cAMP-dependent synaptic plasticity, especially in hippocampal mossy fiber long-term potentiation (LTP) [5].

In cancer research, Syt12 has been shown to act as an oncogene in multiple cancer types. In thyroid carcinoma, its overexpression promotes cancer progression and metastasis, increasing the risk of lymph node metastatic and certain histological types of primary neoplasm [1]. In oral cancer, Syt12 is up-regulated, and its knockdown leads to depressed cellular proliferation, migration, and invasion with cell cycle arrest at G1 phase, potentially via the CAMK2N1 and CAMK2 pathway [2]. In gastric cancer, it may promote the proliferation and migration of cancer cells by inducing epithelial-mesenchymal transition (EMT) [3]. In lung adenocarcinoma, Syt12 expression is increased, associated with advanced tumor stage and reduced prognosis, and it promotes cell proliferation and migration through the PI3K/AKT/mTOR pathway [4].

In conclusion, Syt12 has a crucial function in cAMP-dependent synaptic plasticity in the nervous system. In cancer, it often acts as an oncogene promoting cancer cell proliferation, migration, and invasion in various cancer types such as thyroid, oral, gastric, and lung adenocarcinoma. The study of Syt12 using gene-knockout models in mice has helped to reveal its role in these biological processes and disease conditions, providing potential targets for cancer diagnosis and treatment.