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G2 and S‐phase expressed 1 ( GTSE 1) regulates cell cycle progression in human cancers. However, its significance and mechanism of action in acral melanoma ( AM ) remain unknown. In the present study, we found that  GTSE 1 expression was upregulated in advanced stage/metastatic  AM  tissues and metastatic cell lines, and correlated with higher stage ( P  = .028) and poor disease‐free survival ( DFS ) in patients with  AM  ( P  = .003). Cox regression assays validated  GTSE 1 expression to be an independent prognostic factor of  DFS  for patients with  AM  ( P  = .004). Ectopic expression of  GTSE 1 enhanced primary  AM  cell proliferation, invasion, and migration. Loss‐of‐function in  GTSE 1 attenuated metastatic  AM  cell proliferation and metastatic ability in vitro and in vivo. We additionally observed that inhibition of migration and invasion occurred concomitantly with a  GTSE 1 knockdown‐mediated increase in E‐cadherin and decreases in N‐cadherin and Slug. We further showed that integrin subunit alpha 2 ( ITGA 2) interacts with  GTSE 1 and is a downstream effector of  GTSE 1. Further,  ITGA 2 levels were positively correlated with  GTSE 1 expression in human  AM  tissues. Ectopic  ITGA 2 expression rescued si GTSE 1‐mediated inhibition of migration and invasion, thereby restoring epithelial‐to‐mesenchymal transition ( EMT ). In conclusion,  GTSE 1 expression promotes  AM  progression and correlates with clinical outcomes of patients with  AM , and may represent a promising therapeutic target to suppress  AM  progression.

High G2 and S‐phase expressed 1 expression promotes acral melanoma progression and correlates with poor clinical prognosis