GSN is a protein that is broadly expressed intracellularly, including in the cytoplasm and mitochondria, and exists in both intracellular and an extracellular forms (Wen et al., 1996). Previous studies revealed that the expression of GSN is decreased in many cancers, including NKTCL (Tanaka et al., 2006; Zhou et al., 2016). Deng et al. (2015) showed that the upregulation of GSN promotes cell growth and motility and speculate, which is involved in the progression of human oral cancers. Nevertheless, a study has revealed that overexpression of GSN reduces the proliferation and invasion of colon carcinoma cells (Li et al., 2016). Our study results indicate that GSN overexpression significantly suppressed cell proliferation and invasion in YTS cells. A previous study showed that GSN suppresses apoptosis by negatively regulating the expression of apoptosis-associated genes in hepatocarcinoma cells (Zhou et al., 2015). Our results further showed that overexpression of GSN significantly increased apoptosis in YTS cells. Abedini et al. (2014) revealed that GSN plays roles as both an effector and inhibitor of apoptosis, which underlines its association with a wide variety of cancer types. According to the above results, GSN has different effects on cell proliferation, apoptosis and invasion in different cancers, which may be caused by GSN activating or inactivating different signaling pathways in varying cancers.