Folic Acid Receptor A Facilitates Nasopharyngeal Carcinoma Via Erk1/2/Nf-Kappa B Signaling Pathway

Nasopharyngeal carcinoma (NPC) is an epithelial malignancy with high prevalence in Southeast Asia. Concurrent chemoradiotherapy is the most popular therapeutic method. NPC is mainly characterized by insidious onset and deep lesion site, and thus is difficult to treat. In clinical, the lack of targeted drugs could further affects the therapeutic efficacy for NPC. Folic acid receptor alpha (FR alpha) is an abnormally expressed molecule in various tumor tissues, and is involved in the occurrence and progression of these tumors. However, the potential role and mechanism of FR alpha in NPC remains unclarified. In this study, we detected overexpression of FR alpha in human NPC cell line CNE2 compared with normal nasopharyngeal epithelial cell line NP69 (P<0.05). Further, CNE2 cells were randomly divided into control, scrambled siRNA (negative control) and FR alpha siRNA groups. FR alpha expression was determined by Western blot and real-time PCR analysis. Cell proliferation, invasion and apoptosis were detected by MTT assay, transwell assay, and flow cytometry, respectively. It was found that down-regulation of FR alpha by siRNA significantly inhibited cell proliferation and invasion, but markedly induced cell apoptosis of CNE2 cells compared with control group (all P<0.05). Further mechanism study showed that pERK1/2 and NF-kappa B expression was significantly decreased when compared to control group (P<0.05). In conclusion, our study suggests that FR alpha might facilitate NPC via the ERK1/2/NF-kappa B signaling pathway. FR alpha might be an effective biomarker of NPC and might be useful for the diagnosis and targeted treatment for the malignant disease.