High Expression of Prospero-Related Homeobox-1 (PROX1) Is Associated With Poor Prognosis in Patients With Salivary Adenoid Cystic Carcinoma
- PMID: 29406257
- DOI: 10.1016/j.joms.2017.12.032
High Expression of Prospero-Related Homeobox-1 (PROX1) Is Associated With Poor Prognosis in Patients With Salivary Adenoid Cystic Carcinoma
Abstract
Purpose: Prospero-related homeobox-1 (PROX1) plays an important role in the invasion and metastasis of many human cancers. However, the expression pattern of PROX1 in salivary adenoid cystic carcinoma (SACC) remains unclear. The aim of this study was to investigate PROX1 expression and its prognostic value in SACC.
Materials and methods: PROX1 expression was determined by immunohistochemistry (IHC) in SACC tissue specimens. Correlations between PROX1 expression and clinicopathologic features were investigated. The Kaplan-Meier method was used to analyze the correlation between PROX1 expression and survival. Independent prognostic factors associated with overall survival (OS) were analyzed using Cox regression analysis.
Results: The IHC data showed that the PROX1 positivity rate in SACC tissue specimens was significantly higher than that in normal salivary gland tissues (71.1 vs 13.3%; P < .05). PROX1 expression was detected mainly in the nucleolus. In addition, PROX1 expression was correlated with perineural invasion, local regional recurrence, and distant metastasis of patients with SACC (P < .05), and no significant association was found between PROX1 expression and other clinicopathologic parameters. Data indicated that patients with positive PROX1 expression had poor OS compared with those with negative PROX1 expression (P = .0005). Multivariate analysis showed that PROX1 expression, local regional recurrence, and distant metastasis were independent prognostic factors for OS.
Conclusions: These findings showed that PROX1 expression was statistically higher in SACC specimens. Positive expression of PROX1 might serve as a potential predictor of prognosis in SACC.
Copyright © 2018. Published by Elsevier Inc.
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