Subcellular localization of β-arrestin1 and its prognostic value in lung adenocarcinoma. Issue 45 (November 2017)

• Record Type: Journal Article
• Authors: Li, Xiaowei; Che, Keying; Wang, Liguang; Zhang, Tiehong; Wang, Guanghui; Pang, Zhaofei; Shen, Hongchang; Du, Jiajun
• Other Names: Lawen. Alfons section editor.
• Is Part Of: Medicine. Volume 96:Issue 45(2017)
• Publication Date: 2017-11
• Subjects: β-arrestin1 -- lung adenocarcinoma -- p300 -- prognosis -- subcellular localization; Medicine -- Periodicals; Medicine -- Periodicals; Médecine -- Périodiques; Geneeskunde; Medicine; Periodicals; Periodicals; 610.5
• DOI: 10.1097/MD.0000000000008450
• Languages: English
• ISSNs: 0025-7974

Abstract

Abstract : Abstract: β-Arrestins play important roles in cancer progression, and the subcellular localization of β-arrestin1 has been receiving increasingly more attention. Intriguingly, several studies, including some of our previous work, showed that the effects of β-arrestin1 on outcomes of cancer patients were controversial. Specimens were obtained from 133 patients with lung adenocarcinoma. Immunohistochemistry was used to detect the expression of β-arrestin1 and p300 in the collected tissues. The Kaplan-Meier analysis and Cox proportional hazards regression were used to examine the relationship between β-arrestin1 and patient survival. We found no significant association between β-arrestin1 and clinicopathological variables. The Kaplan-Meier plot showed that patients with high expression of β-arrestin1 (especially in the nucleus) had a poorer overall survival (OS) and shorter disease-free survival (DFS) ( P = .026, P = .015). Additionally, high p300 expression also resulted in worse OS ( P = .039). Following the univariate analysis, high expressions of nuclear β-arrestin1 and p300 were classed as poor prognostic factors for both OS ( P = .016) and DFS ( P = .025). The expression of β-arrestin1 in the nucleus is associated with increased malignant tendency of lung adenocarcinoma, and the predictive value of β-arrestin1 may be optimized by combining information about the expression of p300 acetyltransferase.