Abstract
Nasopharyngeal carcinoma (NPC) is a common tumor in southern China and south-eastern Asia. Effective strategies for the prevention or screening of NPC are limited. Exploring effective biomarkers for the early diagnosis and prognosis of NPC continues to be a rigorous challenge. Evidence is accumulating that DNA methylation alterations are involved in the initiation and progression of NPC. Over the past few decades, aberrant DNA methylation in single or multiple tumor suppressor genes (TSGs) in various biologic samples have been described in NPC, which potentially represents useful biomarkers. Recently, large-scale DNA methylation analysis by genome-wide methylation platform provides a new way to identify candidate DNA methylated markers of NPC. This review summarizes the published research on the diagnostic and prognostic potential biomarkers of DNA methylation for NPC and discusses the current knowledge on DNA methylation as a biomarker for the early detection and monitoring of progression of NPC.
Highlights
Nasopharyngeal carcinoma (NPC) is one of the most prevalent malignancies in southern China and southeastern Asia
Over the past few decades, aberrant DNA methylation in single or multiple tumor suppressor genes (TSGs) in various biologic samples have been described in NPC, which potentially represents useful biomarkers
Abundant evidence convincingly demonstrated that aberrant epigenetic silencing of many tumor suppressor genes (TSGs), cellular functional genes and micro-RNAs affect the normal cell growth and development (Esteller, 2007; Lujambio et al, 2008), which leads to various human malignancies (Belinsky et al, 1998; Mittag et al, 2006), that has been recognized as a common and early event in human cancers(Jones, 1996; Baylin and Herman, 2000)
Summary
Nasopharyngeal carcinoma (NPC) is one of the most prevalent malignancies in southern China and southeastern Asia. From multiple-gene studies, Kwong and colleagues (Kwong et al, 2002) detected the prevalence of several genes methylation in NPC tumors including RARbeta (80%), DAP-kinase (76%), p16 (46%), p15 (17%), p14 (20%), and MGMT (20%), respectively. Detailed mechanistic studies that further elucidated biologic roles in NPC suggested that transcriptional inactivation of different TSGs by promoter hypermethylation is associated with many important cellular processes involved in tumorigenesis. It was recently reported that hypermethylated gene ADAMTS8 plays a promoting role in NPC progression by triggering EGFR-MEK-ERK signaling (Choi et al, 2014) highly methylated gene ROR2 participated in the negative regulation of cell functions through suppressing β-catenin and AKT pathway (Li et al, 2014c). Analyses of DNA methylation provides the opportunity for understanding the molecular pathogenesis of the disease but can be used to develop new potential new markers for diagnosis, prognosis and prediction of NPC
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