Sytl2, or synaptotagmin-like 2, has been implicated in multiple biological processes and disease-related pathways. It appears to play a role in cell mobility-related pathways, potentially influencing processes such as cell migration and invasion. Its function is of significance in understanding tumor metastasis and other disease-associated cellular behaviors [1,3,4].

In prostate cancer, SYTL2 promotes metastasis by enhancing FSCN1-mediated pseudopodia formation. Knockdown of SYTL2 could potentially reverse this effect, suggesting its importance in regulating the mobility of prostate cancer cells [1].

In spinal osteosarcoma, the E2F1-induced lncRNA BSN-AS2 promotes tumor progression by targeting the miR-654-3p/SYTL2 axis. Inhibition of miR-654-3p or overexpression of SYTL2 counteracts the inhibitory effect of BSN-AS2 deficiency on tumor progression [3].

In ovarian cancer, overexpression of SYTL2 promotes metastatic potential, including increased migration and invasiveness in ovarian carcinoma cells [4].

In conclusion, Sytl2 is involved in promoting the metastatic potential of cancer cells, such as in prostate, spinal osteosarcoma, and ovarian cancers. The study of Sytl2 through various functional experiments helps in understanding the mechanisms of cancer metastasis, providing potential targets for cancer treatment. Additionally, its role in other diseases like thoracic aortic aneurysm as a diagnostic marker gene, and its association with genes in NK cell-related signaling pathways in sleep-deprivation-related myocardial infarction, further highlight its significance in different disease areas [2,5].