肿瘤干细胞是一小部分具有干细胞样特性的肿瘤细胞，是肿瘤治疗抵抗和复发的根源。miR-124在鼻咽癌细胞增殖及治疗抵抗等方面起了重要作用，是鼻咽癌重要调节因子之一。结合黏附分子家族蛋白A（Junctional adhesion molecule A, JAMA）能促进乳腺癌、肝癌和结直肠癌细胞的增殖并标记造血干细胞。我们研究已经证实JAMA能促进鼻咽癌细胞上皮间充质转化，并与患者不良预后密切相关。前期的生物信息学预测结果显示miR-124能靶向作用于JAMA。因此，我们假设：miR-124通过靶向作用于JAMA抑制鼻咽癌干细胞。我们首先通过体内及体外实验验证miR-124对鼻咽癌干细胞影响；进一步阐明其作用机制：miR-124靶向作用于JAMA，通过Akt信号通路抑制鼻咽癌干细胞；探讨miR-124与鼻咽癌临床病理的相关性。这将为明确鼻咽癌放疗抵抗机制和确定新的治疗靶点提供理论和实践基础。

Nasopharyngeal carcinoma (NPC) is an endemic disease in southern China and Southeast Asia. A major impediment to achieve long-term survival is radioresistance and local recurrence. Therefore, it is important to understand the mechanisms of radioresistance to develop more specific treatment for NPC and improve patient prognosis. Cancer stem cells (CSCs) are defined as a subpopulation of tumor cells having stem cell-like properties. It has been considered that CSCs might be responsible for cancers’ relapse and resistance to treatment. MiR-124 plays an important role in NPC by suppressing tumor proliferation. JAMA is a novel cell-surface marker for long-term repopulating hematopoietic stem cells, which can promote cell proliferation of breast cancer, hepatocellular carcinoma and colorectal cancer. Our results have indicated that JAMA, an epithelial-mesenchymal transition inducer, correlated with metastasis and poor prognosis in human NPC. Furthermore, our preliminary results from bioinformatics have confirmed that miR-124 targeted directly JAMA. Therefore, we hypothesized that miR-124 inhibit human CSCs of NPC by targeting JAMA. Firstly, the effect of JAMA on CSCs will be investigated in vitro and in vivo. Then, the mechanism of miR-124 inhibiting human CSCs of NPC will be studied. Finally clinical significance of JAMA expression in patients with cancer were performed. These results will provide a new insight into the mechanism of resistance to treatment and provide the basis to explore new effective treatment modalities for NPC patients.