Abstract
Globally, thyroid cancer (TC) is considered to be the commonest endocrine malignancy. GINS complex subunit 2 (GINS2) belongs to the GINS complex family and is associated with cellular migration, invasion and growth. The present study aimed to investigate the underlying mechanisms of GINS2 on cell viability, migration and invasion in TC cells. By using MTT, wound healing and Transwell assays, the cell viability, migration and invasion were determined. Apoptosis was examined by immunofluorescence. Western blotting was used to detect protein expression levels. In the present study, biological function analysis demonstrated that GINS2 interference attenuated cell viability, migration and invasion in TC cell lines (K1 and SW579). It was discovered that, compared with the control group, GINS2 silencing induced apoptosis in TC cells. Additionally, GINS2 interference inhibited key proteins in the MAPK signaling pathway, including JNK, ERK and p38. According to these comparative experiments, GINS2 was considered to act a pivotal part in cell viability, migration and invasion of TC by regulating the MAPK signaling pathway and might be a potential therapeutic target for treating TC.