Abstract
Abstract Purpose: Each year in the United States there are more than 65,000 Americans diagnosed with head and neck cancer and 25,000 die from this disease. Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous disease with complex molecular abnormalities, including overexpression of epidermal growth factor receptor (EGFR). The overexpression of EGFR is seen in 80-90% of HNSCC cases and has been shown to be an indicator of poor prognosis and survival in oral cancer patients. The molecular mechanism of EGFR gene expression is poorly understood in HNSCC. MicroRNAs are a new class of posttranslational regulators of gene expression and are a useful target in understanding EGFR gene expression in HNSCC. We hypothesize that microRNAs may play an important role in EGFR gene overexpression during HNSCC processes. Design Methods: We generated stably expressing exogenous miRNA-7 or miRNA-128 in cell lines (JHU-06,-011,-013,-019, -022, and -029 using lentivirus infection, performed colony formation assays to determine cell growth and proliferation, QRT-PCR to analyze gene expression, and Western blot analysis to evaluate protein expression. Results: We found that the miR-7 and -128 transfection efficiency were quite different in these six cell lines. The transfected cell lines stably expressed exogenous miR-7 or -128. Compared with the control cells, the levels of EGFR protein and cell viability were significantly lower in miR-7, -128 transfected HNSCC cell lines. CONCLUSION: We successfully constructed the stably expressing exogenous miR-7, -128 HNSCC cell lines and validated that miR-7,-128 can down-regulate EGFR expression by specifically targeting the EGFR mRNA 3’UTR. MiR-7 and miR-128 have potential to serve as a therapeutic approach to specifically target EGFR in HNSCC. This work was supported in part by grants P20 CA118770 from National Cancer Institute. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3949. doi:10.1158/1538-7445.AM2011-3949
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