Cytoplasmic polyadenylation element-binding protein-4 (CPEB4) is involved in several biological processes that are associated with cancer progression. However, it remains unknown whether CPEB4 expression levels are associated with head and neck squamous cell carcinoma (HNSCC). The aim of the present study was to explore the potential function of CPEB4 in HNSCC. The expression of CPEB4 was analyzed in HNSCC from six Gene Expression Omnibus (GEO) datasets. Immunohistochemical staining was conducted to examine CPEB4 protein levels in an HNSCC tissue microarray (TMA). According to the GEO dataset analyses, gene expression was downregulated in HNSCC compared with normal samples (P<0.05). Notably, a statistical difference was observed between different tumor grades (P<0.05). Furthermore, the methylation of the gene in HNSCC was significantly increased compared with that observed in normal samples (P<0.01). The outcome from the TMA demonstrated that CPEB4 protein expression in human HNSCC tumors was significantly decreased compared with normal samples (P<0.05). In addition, the expression of CPEB4 protein was negatively associated with histological grades of HNSCC (P<0.05). The results from the present study suggested that CPEB4 may function as a tumor suppressor gene in HNSCC, which identifies the potential value of CPEB4 in predicting prognosis of HNSCC. Hypermethylation of the gene may be responsible for the downregulation of CPEB4 expression in HNSCC and result in tumorigenesis.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5778832PMC
http://dx.doi.org/10.3892/ol.2017.7661DOI Listing

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Article Synopsis
  • - Alternative splicing includes microexons in neuronal proteins, which are often linked to neurodevelopmental disorders, including autism spectrum disorder (ASD).
  • - A specific 24-nucleotide microexon in the RNA-binding protein CPEB4, previously shown to be less included in individuals with ASD, plays a critical role in regulating gene expression linked to neurodevelopment.
  • - The study finds that this microexon helps maintain the flexible regulation of CPEB4 during neuronal activation by preventing its aggregation, allowing it to switch from repressing to activating translation of genes.
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