Abstract

Nasopharyngeal carcinoma (NPC) is a malignancy of epithelial origin that is prone to local invasion and early distant metastasis. Although concurrent chemotherapy and radiotherapy improves the 5-year survival outcomes, persistent or recurrent disease still occurs. Therefore, novel therapeutic targets are needed for NPC patients. MicroRNAs (miRNAs) play important roles in normal cell homeostasis, and dysregulations of miRNA expression have been implicated in human cancers. In NPC, studies have revealed that miRNAs are dysregulated and involved in tumorigenesis, metastasis, invasion, resistance to chemo- and radiotherapy, and other disease- and treatment-related processes. The advantage of miRNA-based treatment approaches is that miRNAs can concurrently target multiple effectors of pathways involved in tumor cell differentiation and proliferation. Thus, miRNA-based cancer treatments, alone or combined with standard chemotherapy and/or radiotherapy, hold promise to improve treatment response and cure rates. In this review, we will summarize the dysregulation of miRNAs in NPC initiation, progression, and treatment as well as NPC-related signaling pathways, and we will discuss the potential applications of miRNAs as biomarkers and therapeutic targets in NPC patients. We conclude that miRNAs might be potential promising therapeutic targets in nasopharyngeal carcinoma.

Highlights

  • Nasopharyngeal Carcinoma (NPC)Nasopharyngeal carcinoma is a non-lymphomatous squamous cell carcinoma that arises from the epithelial lining of the nasopharynx

  • Local invasion and early distant metastasis are common in NPC

  • Concurrent chemotherapy and radiotherapy is a standard treatment for late-stage NPC [3]

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Summary

Introduction

Nasopharyngeal Carcinoma (NPC)Nasopharyngeal carcinoma is a non-lymphomatous squamous cell carcinoma that arises from the epithelial lining of the nasopharynx. Tumor suppressor genes are usually inhibited by miRNAs directly, and such miRNAs are considered to be oncomiRNAs. For example, cell cycle inhibitor CDKN1A ( called P21) is believed to be directly targeted by miR-663 in NPC, leading to the promotion of NPC cell proliferation and tumorigenesis [43].

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