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However, its significance and mechanism of action in acral melanoma (AM<\/jats:styled-content>) remain unknown. In the present study, we found that GTSE<\/jats:styled-content>1 expression was upregulated in advanced stage\/metastatic AM<\/jats:styled-content> tissues and metastatic cell lines, and correlated with higher stage (P<\/jats:italic>\u00a0=\u00a0.028) and poor disease\u2010free survival (DFS<\/jats:styled-content>) in patients with AM<\/jats:styled-content> (P<\/jats:italic>\u00a0=\u00a0.003). Cox regression assays validated GTSE<\/jats:styled-content>1 expression to be an independent prognostic factor of DFS<\/jats:styled-content> for patients with AM<\/jats:styled-content> (P<\/jats:italic>\u00a0=\u00a0.004). Ectopic expression of GTSE<\/jats:styled-content>1 enhanced primary AM<\/jats:styled-content> cell proliferation, invasion, and migration. Loss\u2010of\u2010function in GTSE<\/jats:styled-content>1 attenuated metastatic AM<\/jats:styled-content> cell proliferation and metastatic ability in\u00a0vitro and in\u00a0vivo. We additionally observed that inhibition of migration and invasion occurred concomitantly with a GTSE<\/jats:styled-content>1 knockdown\u2010mediated increase in E\u2010cadherin and decreases in N\u2010cadherin and Slug. We further showed that integrin subunit alpha 2 (ITGA<\/jats:styled-content>2) interacts with GTSE<\/jats:styled-content>1 and is a downstream effector of GTSE<\/jats:styled-content>1. Further, ITGA<\/jats:styled-content>2 levels were positively correlated with GTSE<\/jats:styled-content>1 expression in human AM<\/jats:styled-content> tissues. Ectopic ITGA<\/jats:styled-content>2 expression rescued siGTSE<\/jats:styled-content>1\u2010mediated inhibition of migration and invasion, thereby restoring epithelial\u2010to\u2010mesenchymal transition (EMT<\/jats:styled-content>). In conclusion, GTSE<\/jats:styled-content>1 expression promotes AM<\/jats:styled-content> progression and correlates with clinical outcomes of patients with AM<\/jats:styled-content>, and may represent a promising therapeutic target to suppress AM<\/jats:styled-content> progression.<\/jats:p>","DOI":"10.1111\/cas.13607","type":"journal-article","created":{"date-parts":[[2018,4,16]],"date-time":"2018-04-16T23:34:39Z","timestamp":1523921679000},"page":"1787-1798","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["High G2 and S\u2010phase expressed 1 expression promotes acral melanoma progression and correlates with poor clinical prognosis"],"prefix":"10.1111","volume":"109","author":[{"given":"Tianxiao","family":"Xu","sequence":"first","affiliation":[{"name":"Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education\/Beijing) Department of Renal Cancer and Melanoma Peking University Cancer 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