Abstract
A low NM23-H1 expression in head and neck squamous cell carcinoma (HNSCC) was found to be associated with poor clinical outcome. Therefore, we investigated the role of NM23-H1 in the susceptibility of HNSCC cells to irradiation and its clinical significance. An in vitro study was also conducted to validate the results. Furthermore, we used immunohistochemistry to analyze NM23-H1 expression found in specimens of 50 HNSCC patients with cervical metastases receiving postoperative radiotherapy. Low tumor NM23-H1 expression was associated with locoregional recurrence of HNSCC (p=0.040; Hazard ratio=5.62) and poor clinical outcome (p=0.001; Hazard ratio=4.90). To confirm the effect of NM23-H1 on radiation-induced cytotoxicity, we generated several stable clones derived from a human HNSCC cell line (SAS) using knockdown and overexpression of NM23-H1. Knockdown of NM23-H1 decreased the radio-sensitivity of SAS cells, possibly associated with a decrease in the radiation-induced G2/M-phase accumulation and upregulation of cyclin B1. On the contrary, overexpression of NM23-H1 can reverse the aforementioned adverse results. Consequently, we suggest that NM23-H1 expression may be considered as a potential therapeutic treatment option for HNSCC patients.
Highlights
The prevalence of Head and neck cancers (HNC), mainly squamous cell carcinomas (HNSCC), are increasing worldwide [1]
In order to understand the role of NM23-H1 in prognosis of head and neck squamous cell carcinoma (HNSCC) patients with cervical metastases treated by surgery and postoperative irradiation, we inspected the NM23-H1 expression found in the specimens
The salient findings of this study showed low NM23-H1 expression in primary tumors was associated with locoregional recurrence in HNSCC patients with cervical metastases receiving surgery and radiotherapy
Summary
The prevalence of Head and neck cancers (HNC), mainly squamous cell carcinomas (HNSCC), are increasing worldwide [1]. Most HNSCC patients with potentially removable tumors have lymphatic metastases at the time of their diagnosis [2]. There are no useful biomarkers for treatment planning for HNSCC patients with metastases. Low NM23-H1 expression is long known to be associated with therapeutic resistance and metastasis in some cancers [3,4,5,6]. Clinical observation on NM23-H1 expression in treatment outcome of various cancers had yielded inconsistent results [7,8,9,10]. The survival mechanism of spreading cells was the major contributor to therapeutic resistance of recurrent tumors [4]. Restoring NM23-H1 expression might lead to better treatment outcome of residual cancer cells [13]
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