Overexpression of EGFR in Head and Neck Squamous Cell Carcinoma Is Associated with Inactivation of SH3GL2 and CDC25A Genes
Overexpression of EGFR in Head and Neck Squamous Cell Carcinoma Is Associated with Inactivation of SH3GL2 and CDC25A Genes
The aim of this study is to understand the mechanism of EGFR overexpression in head and neck squamous cell carcinoma (HNSCC). For this reason, expression/mutation of EGFR were analyzed in 30 dysplastic head and neck lesions and 148 HNSCC samples of Indian patients along with 3 HNSCC cell lines. In addition, deletion/methylation/mutation/expression of SH3GL2 (associated with EGFR degradation) and CDC25A (associated with dephosphorylation of EGFR) were analyzed in the same set of samples. Our study revealed high frequency of EGFR overexpression (66-84%), low frequency of gene amplification (10-32.5%) and absence of functional mutation in the dysplastic lesions and HNSCC samples. No correlation was found between protein overexpression and mRNA expression/gene amplification status of EGFR. On the other hand, frequent alterations (deletion/methylation) of SH3GL2 (63-77%) and CDC25A (37-64%) were seen in the dysplastic and HNSCC samples. Two novel single nucleotide polymorphism (SNPs) were found in the promoter region of SH3GL2. Reduced expression of these genes showed concordance with their alterations. Overexpression of EGFR and p-EGFR were significantly associated with reduced expression and alterations of SH3GL2 and CDC25A respectively. In-vitro demethylation experiment by 5-aza-2'-deoxycytidine (5-aza-dC) showed upregulation of SH3GL2 and CDC25A and downregulation of EGFR expression in Hep2 cell line. Poor patient outcome was predicted in the cases with alterations of SH3GL2 and CDC25A in presence of human papilloma virus (HPV) infection. Also, low SH3GL2 and high EGFR expression was a predictor of poor patient survival. Thus, our data suggests that overexpression of EGFR due to its reduced degradation and dephosphorylation is needed for development of HNSCC.
- Council of Scientific and Industrial Research India
- Johns Hopkins Medicine United States
- Chittaranjan National Cancer Institute India
- Johns Hopkins University United States
- Indian Institute of Chemical Biology India
Adult, Science, Gene Expression, Humans, cdc25 Phosphatases, Gene Silencing, Promoter Regions, Genetic, Papillomaviridae, Adaptor Proteins, Signal Transducing, Aged, Squamous Cell Carcinoma of Head and Neck, Q, R, Gene Amplification, Reproducibility of Results, DNA Methylation, Middle Aged, ErbB Receptors, Gene Expression Regulation, Neoplastic, Head and Neck Neoplasms, Mutation, Carcinoma, Squamous Cell, Medicine, Gene Deletion, Research Article
Adult, Science, Gene Expression, Humans, cdc25 Phosphatases, Gene Silencing, Promoter Regions, Genetic, Papillomaviridae, Adaptor Proteins, Signal Transducing, Aged, Squamous Cell Carcinoma of Head and Neck, Q, R, Gene Amplification, Reproducibility of Results, DNA Methylation, Middle Aged, ErbB Receptors, Gene Expression Regulation, Neoplastic, Head and Neck Neoplasms, Mutation, Carcinoma, Squamous Cell, Medicine, Gene Deletion, Research Article
47 Research products, page 1 of 5
- 2017IsRelatedTo
- 2017IsRelatedTo
- 2017IsRelatedTo
- 2017IsRelatedTo
- 2017IsRelatedTo
- 2017IsRelatedTo
- 2017IsRelatedTo
- 2017IsRelatedTo
chevron_left - 1
- 2
- 3
- 4
- 5
chevron_right
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).73 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Top 10% influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Top 10% impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Top 10%
