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Subcellular localization of β-arrestin1 and its prognostic value in lung adenocarcinoma

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 contr...

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Detalles Bibliográficos
Autores principales: Li, Xiaowei, Che, Keying, Wang, Liguang, Zhang, Tiehong, Wang, Guanghui, Pang, Zhaofei, Shen, Hongchang, Du, Jiajun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5690724/
https://www.ncbi.nlm.nih.gov/pubmed/29137031
http://dx.doi.org/10.1097/MD.0000000000008450
Descripción
Sumario: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.